Materiały źródłowe

• #1 Trichomonas vaginalis: Pathogenesis, Symbiont Interactions, and Host Cell Immune Responses – PubMed

  https://pubmed.ncbi.nlm.nih.gov/30056833/

  The parasite Trichomonas vaginalis (Tv) causes a highly prevalent sexually transmitted infection. As an extracellular pathogen, the parasite mediates adherence to epithelial cells to colonize the human host. […] Modes of Tv pathogenesis include damage to host tissue mediated by parasite killing of host cells, disruption of steady-state vaginal microbial ecology, and eliciting inflammation by activating the host immune response. […] Mechanisms that may lead to parasite recognition and killing, or the evasion of host immune cells, have also been revealed.

• #2 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. […] However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. […] The factors considered to be involved in the pathogenicity of T. vaginalis include; the ability of trichomonads to adhere to vaginal epithelial cells (VECs), the cytotoxic effect of the pathogen on host cells, trichomonad proteinase activity, and the ability of trichomonads to produce subcutaneous abscess lesions in mice. […] In terms of the pathogenesis of T. vaginalis, parasite attachment to host cells is a prerequisite for the establishment of infection, as the organism must overcome constant vaginal secretions.

• #3 KoreaMed Synapse

  https://synapse.koreamed.org/articles/1044052

  Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. […] We investigated that trichomonads in the vagina sometime after an acute infection secrete proteins like excretory-secretory product that have a chemotactic effect on neutrophils, and that these neutrophils are further stimulated by T. vaginalis to produce chemokines like IL-8 and GRO-, which further promote neutrophil recruitment and chemotaxis. Thus, neutrophil accumulation is believed to maintain or aggravate inflammation. […] However, enhanced neutrophil apoptosis induced by live T. vaginalis could contribute to resolution of inflammation via anti-inflammatory cytokine produced by human macrophage phagocytosed of apoptotic neutrophils. Macrophages may constitute an important component of host defense against T. vaginalis infection, and may be involved in inflammation via production of proinflammatory cytokines and nitric oxide. […] In the host, T. vaginalis uses a capping phenomenon and cleave host immunoglobulins with proteinases as the evasion methods from host immune responses. […] The mechanisms and molecules involved in cytoadherence and pathogenesis of T. vaginalis.

• #4 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  Trichomonas vaginalis is the etiologic agent of trichomoniasis, the most common non-viral sexually transmitted disease (STD) in the world. […] To achieve success in parasitism trichomonads develop a complex process against the host cells that includes dependent- and independent-contact mechanisms. This multifactorial pathogenesis includes molecules such as soluble factors, secreted proteinases, adhesins, lipophosphoglycan that culminate in cytoadherence and cytotoxicity against the host cells. […] The T. vaginalis infection is very complex with a broad range of symptoms which may be attributed to distinct pathogenic process mediated by the parasite through contact-dependent and -independent mechanisms. The colonization of the infection site is initiated when the parasite triggers cellular damage in the host tissue by secreting a wide variety of molecules, known as cytolytic factors. Trichomonas vaginalis factor (TvF), a 250 kDa cytolytic effector, causes cell rounding and clumping without lysis. Another soluble factor released into the medium by the parasite in contact with cells is a glycoprotein with 200 kDa, known as cell-detaching factor (CDF) which promotes cell detachment.

• #5 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  Human trichomonosis, infection with Trichomonas vaginalis, is the most common non-viral sexually transmitted disease in the world. The host-parasite interaction and pathophysiological processes of trichomonosis remain incompletely understood. This review focuses on the advancements reached in the area of the pathogenesis of T. vaginalis, especially in the role of the cysteine proteinases. It highlights various approaches made in this field and lists a group of trichomonad cysteine proteinases involved in diverse processes such as invasion of the mucous layer, cytoadherence, cytotoxicity, cytoskeleton disruption of red blood cells, hemolysis, and evasion of the host immune response. […] The exact mechanisms of the pathogenesis have not been clearly elucidated to date. However, the sequencing of the T. vaginalis genome has led to knowledge of new gene families involved in the host pathogenesis, leading to new research to understand the mechanism of the parasites pathogenicity better. Trichomonal cytoadherence to epithelial cells is a critical step in the initiation phase of the infection and subsequent pathogenesis.

• #6 Trichomoniasis – symptoms, diagnosis and treatment in Kyiv at the Universum Clinic private clinic

  https://universum.clinic/en/service/zagalni-napryamki/ginekologiya/trykhomonyaz/

  This disease exhibits several characteristics that experienced dermatovenereologists are aware of and take into account: […] High infectivity: Trichomonas vaginalis has specific receptors on its surface, which allow it to bind to human epithelial cells within a few minutes after infection. […] Significant virulence: Trichomonads destroy red blood cells, reduce the activity of tissue immunity, and create a gateway for other STI agents. […] Resistance to the immune response: Immune cells are unable to eliminate the pathogens and may perish, leading to a subacute inflammatory process. […] Propensity for a chronic course: Infections often have subtle, hidden symptoms, but infected individuals can transmit the disease, particularly through unprotected sexual contact.

• #7 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The multifactorial nature of trichomonal pathogenesis also involves a sequence of events, where contact-dependent mechanisms play crucial roles. Upon contact with host cells, the parasite undergoes a drastic morphological shift. The free-swimming piriform trophozoites transform into an ameboid form leading to a tight association to the target cells. […] The mechanisms of cell adhesion are extensively studied in the parasite and up to now three major classes of molecules show evidence to be involved in the cytoadherence: lipophosphoglycan, adhesins and a collection of membrane proteins that have been recently identified through genomics and proteomics. […] The T. vaginalis lipophosphoglycan (TvLPG) is one of the most abundant components of the glycocalyx the outer layer of the cell membrane formed by different carbohydrate-associated molecules that binds to galectin-1 and -3 receptors in the host cells.

• #8 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The multifactorial nature of trichomonal pathogenesis also involves a sequence of events, where contact-dependent mechanisms play crucial roles. Upon contact with host cells, the parasite undergoes a drastic morphological shift. The free-swimming piriform trophozoites transform into an ameboid form leading to a tight association to the target cells. […] The mechanisms of cell adhesion are extensively studied in the parasite and up to now three major classes of molecules show evidence to be involved in the cytoadherence: lipophosphoglycan, adhesins and a collection of membrane proteins that have been recently identified through genomics and proteomics. […] The T. vaginalis lipophosphoglycan (TvLPG) is one of the most abundant components of the glycocalyx the outer layer of the cell membrane formed by different carbohydrate-associated molecules that binds to galectin-1 and -3 receptors in the host cells.

• #9 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The multifactorial nature of trichomonal pathogenesis also involves a sequence of events, where contact-dependent mechanisms play crucial roles. Upon contact with host cells, the parasite undergoes a drastic morphological shift. The free-swimming piriform trophozoites transform into an ameboid form leading to a tight association to the target cells. […] The mechanisms of cell adhesion are extensively studied in the parasite and up to now three major classes of molecules show evidence to be involved in the cytoadherence: lipophosphoglycan, adhesins and a collection of membrane proteins that have been recently identified through genomics and proteomics. […] The T. vaginalis lipophosphoglycan (TvLPG) is one of the most abundant components of the glycocalyx the outer layer of the cell membrane formed by different carbohydrate-associated molecules that binds to galectin-1 and -3 receptors in the host cells.

• #10

  https://www-.grantome.com/grant/NIH/R01-AI069058-04

  Trichomonas vaginalis is the etiologic agent of the most common non-viral sexually transmitted infection (STI) worldwide and is the most prevalent parasite found in the US population. […] Despite its global medical importance, the molecular mechanisms underlying the pathogenesis of T. vaginalis are virtually unknown. […] We have demonstrated a role for the glycocalyx that coats the surface of this parasite in host cell adherence and cytotoxicity and have identified the first putative host cell receptor for T. vaginalis. […] To this end, we propose to (1) elucidate the structure of wild-type and mutant T. vaginalis surface glycoconjugates and lipophosphoglycan (LPG) as a step towards identifying novel enzymes involved in its assembly, (2) delete the serine palmitoyl transferase 2 (SPT2) gene to create LPG null mutants and determine the effect on adherence and cytotoxicity of the parasite (3) validate candidate T. vaginalis genes required for the synthesis and assembly of the monosaccharide rhamnose, an unusual sugar that is absent in host cells and (4) examine the interaction between T. vaginalis LPG and host cell galectin-1 (gal-1) and investigate whether this interaction plays a role in pathogenesis. […] In addition to providing critical data on the mechanisms underlying host-pathogen interaction of this prevalent STI, the proposed studies will yield information that may be useful for developing novel drug therapies and vaccination strategies.

• #11 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The second class of T. vaginalis proteins related to adherence comprises the named adhesins five proteins (AP120, AP65, AP51, AP33, and AP23) that apart from AP23, are abundant metabolic enzymes primarily involved in carbohydrate metabolism and found in the hydrogenosome. […] Another important factor contributing to T. vaginalis pathogenesis is the high cytotoxic potential of the parasite. Its ability to promote cytolysis followed by phagocytosis is what triggers the disruption of cell monolayers. […] The host defense in response to T. vaginalis infection involves multiple mechanisms such as non-immunological factors, non-specific and specific mechanisms of the innate immune response. […] Despite all the immune responses mediated by the host cells, T. vaginalis is able to evade those mechanisms and displays the whole pathogenic potential which turns trichomoniasis a chronic and persistent infection.

• #12

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  Although T. vaginalis is the most common cause of nonviral STD, the exact mechanism of its pathogenesis has not been clearly elucidated. […] Many mechanisms are thought to be involved and all the pathogenic mechanisms (i.e., contact-dependent, contact-independent, and immune response) are probably important in the virulence of this disease. […] The adhesion of the parasite to the epithelial cells seems to be mediated by four adhesion proteins: AP65, AP51, AP33, and AP23, which act in a specific receptor-ligand fashion, dependent on time, temperature, and pH. […] Gene expression of the four adhesion proteins is coordinately upregulated at the transcriptional level by iron. […] Adherence, however, does not correlate directly with virulence, since virulent strains isolated from symptomatic patients exhibited wide differences in their ability to adhere to host cells.

• #13 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The multifactorial nature of trichomonal pathogenesis also involves a sequence of events, where contact-dependent mechanisms play crucial roles. Upon contact with host cells, the parasite undergoes a drastic morphological shift. The free-swimming piriform trophozoites transform into an ameboid form leading to a tight association to the target cells. […] The mechanisms of cell adhesion are extensively studied in the parasite and up to now three major classes of molecules show evidence to be involved in the cytoadherence: lipophosphoglycan, adhesins and a collection of membrane proteins that have been recently identified through genomics and proteomics. […] The T. vaginalis lipophosphoglycan (TvLPG) is one of the most abundant components of the glycocalyx the outer layer of the cell membrane formed by different carbohydrate-associated molecules that binds to galectin-1 and -3 receptors in the host cells.

• #14

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  Although T. vaginalis is the most common cause of nonviral STD, the exact mechanism of its pathogenesis has not been clearly elucidated. […] Many mechanisms are thought to be involved and all the pathogenic mechanisms (i.e., contact-dependent, contact-independent, and immune response) are probably important in the virulence of this disease. […] The adhesion of the parasite to the epithelial cells seems to be mediated by four adhesion proteins: AP65, AP51, AP33, and AP23, which act in a specific receptor-ligand fashion, dependent on time, temperature, and pH. […] Gene expression of the four adhesion proteins is coordinately upregulated at the transcriptional level by iron. […] Adherence, however, does not correlate directly with virulence, since virulent strains isolated from symptomatic patients exhibited wide differences in their ability to adhere to host cells.

• #15 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  T. vaginalis is a parasitic pathogen primarily infecting squamous epithelial cells of the human genital tract, causing damage to these cells. […] It has its own microbiota, harboring two Mycoplasma species and a double-stranded RNA virus, T. vaginalis virus (TVV), which can contribute to its pathogenesis. […] TVV2 and TVV3 to surface expression of an immunogenic protein, P270, which is associated with cytotoxicity, cytoadherence, and host immune evasion. […] The greater likelihood of persistence in women is linked to greater availability of iron, an essential nutrient. […] Menstrual blood creates a rich growth medium which promotes attachment and growth of the parasite in the vaginal canal. […] The physiological mechanisms linking T. vaginalis and adverse birth outcomes are not well understood. One hypothesis is that PTD and PROM in T. vaginalis-infected pregnant women are related to maternal innate immune inflammatory responses to the parasite, which involve elevated cervical interleukin-8 (IL-8) and vaginal defensin levels.

• #16

  https://link.springer.com/article/10.1007/s004360050066

  The mechanism of cytopathogenicity of Trichomonas vaginalis is not well established. Adhesion of T. vaginalis to human epithelial cells is considered a prerequisite for parasitic infection and its pathogenic effect. […] Analysis of the electron microscope data showed that T. vaginalis established contact with the host cells as early as after 6 h of incubation; however, a close attachment of parasites to the epithelial cells occurred only after 9 h. Amoeboid T. vaginalis formed numerous cytoplasmic extensions and adhered to the epithelial cells mostly through the portions of their body opposite the undulating membrane. A dense network of microfilaments was seen at the site of contact between T. vaginalis and epithelial cells. Damaged and desquamated epithelial cells were seen with TEM and SEM only in the areas where parasites were in direct contact with target cells.

• #17 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-is-Trichomoniasis.aspx

  Although pathogenesis and virulence of Trichomonas vaginalis in the progression of trichomoniasis is not fully elucidated, substantial progress has been achieved in identifying products of this protozoan that can damage host tissues and cells. […] Two different schools of thought coexist regarding the pathogenesis of Trichomonas vaginalis contact-dependent and contact-independent. It is very likely that both mechanisms are important in the development of infection. […] In any case, the adhesion process is pivotal in the onset of trichomoniasis, as it triggers the degradation of the cell membrane skeleton and subsequent cytolysis (or disintegration of the cell). […] Recent research endeavors suggest that Trichomonas has the ability to produce molecules that target cells and confer cytotoxicity by damaging cell plasma membrane. One such molecule can create pores in the membranes of erythrocyte membranes (which was detected by using electron microscopy), thereby exhibiting perforin-like activity.

• #18

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  On the other hand, the hemolytic activity of the parasite appears to be correlated with virulence. […] The contact-dependent mechanisms described above play an important role in the pathogenesis of the disease. […] There are reports of other parasite products, described as cell-detaching factors (CDF), that are released by the parasite and are known to have trypsin-like activity. […] The rise of vaginal pH during trichomoniasis may therefore be crucial in the pathogenesis of the disease. […] The relationship between protective lactobacilli and T. vaginalis is not completely understood. […] T. vaginalis has numerous ways of evading the immune system, which include evasion of complement-mediated destruction, molecular mimicry, and the ability to coat itself with host plasma proteins.

• #19 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  T vaginalis destroys epithelial cells by direct cell contact and by the release of cytotoxic substances. […] It also binds to host plasma proteins, thereby preventing recognition of the parasite by the alternative complement pathway and host proteinases. During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs are the predominant host defense mechanism against T vaginalis and respond to chemotactic substances released by trichomonads. […] Despite the immune systems interaction with T vaginalis, infection produces an immunity that is only partially protective at best, and there is little evidence that a healthy immune system prevents infection. […] One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV-infected women.

• #20 Trichomonas vaginalis: pathogenesis and its role in cervical cancer

  http://ve.scielo.org/scielo.php?script=sci_arttext&pid=S0535-51332020000400349

  Trichomonas vaginalis: pathogenesis and its role in cervical cancer […] The objective of this article was to review and to analyze the possible role that Trichomonas vaginalis has as a co-factor in the origin and development of cervical cancer. […] This review article analyzes the possible mechanisms that Trichomonas vaginalis could play in the carcinogenesis of the cervical cancer as a co-factor with the human papilloma virus or as an independent factor. […] Tv primarily infects the squamous epithelium of the female and male urogenital tract. […] The parasite adheres to the wall of the cervicovaginal cells and, by a very effective enzyme system, it interferes in the metabolism of the host generating toxins that may lead to cell necrosis. […] The high density of lipophosphoglycans (LPGs) on the parasite surface suggests that they have important roles in parasite biology and in the infections they cause. […] Fichorova et al. confirmed the role of surface carbohydrates in the adhesion of Tv to host epithelial cells in the lower female genital tract and strengthen the evidence of LPG involvement in this process.

• #21 Trichomoniasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK534826/

  Trichomonas is a motile organism with a size comparable to a white blood cell. It has at least 4 flagella that provide undulating motility. The organism resides in the lumen of the urogenital tract. The organism releases cytotoxic proteins that destroy the epithelial lining. During an infection, the vaginal pH usually increases. […] In women, T. vaginalis has an incubation period of five to twenty-eight days. Women with trichomoniasis often complain of a foul-smelling yellow or green vaginal discharge, dyspareunia, urinary frequency, dysuria, and/or vulvar pruritus or erythema. In men, it often does not cause symptoms. If a male is symptomatic, the most common symptom is urethritis. Less commonly, men may also develop prostatitis and epididymitis.

• #22 Trichomoniasis

  https://www.csh.org.tw/dr.tcj/educartion/f/web/Trichomoniasis/index.htm

  Trichomoniasis is a sexually transmitted protozoal infection caused by Trichomonas vaginalis. […] In women, T vaginalis is isolated from the vagina, cervix, urethra, bladder, and Bartholin and Skene glands. In men, the organism is isolated from the anterior urethra, external genitalia, prostate, epididymis, and semen. […] The protozoan pathogen causes direct damage to the epithelium, leading to microulcerations. […] The mechanism of action is not well understood; however, it is known that anaerobic organisms preferentially reduce the 5-nitro group and active metabolites likely interact with anaerobic bacterial and protozoal DNA.

• #23 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  Trichomonas vaginalis is the etiologic agent of trichomoniasis, the most common non-viral sexually transmitted disease (STD) in the world. […] To achieve success in parasitism trichomonads develop a complex process against the host cells that includes dependent- and independent-contact mechanisms. This multifactorial pathogenesis includes molecules such as soluble factors, secreted proteinases, adhesins, lipophosphoglycan that culminate in cytoadherence and cytotoxicity against the host cells. […] The T. vaginalis infection is very complex with a broad range of symptoms which may be attributed to distinct pathogenic process mediated by the parasite through contact-dependent and -independent mechanisms. The colonization of the infection site is initiated when the parasite triggers cellular damage in the host tissue by secreting a wide variety of molecules, known as cytolytic factors. Trichomonas vaginalis factor (TvF), a 250 kDa cytolytic effector, causes cell rounding and clumping without lysis. Another soluble factor released into the medium by the parasite in contact with cells is a glycoprotein with 200 kDa, known as cell-detaching factor (CDF) which promotes cell detachment.

• #24 Trichomoniasis

  https://www.csh.org.tw/dr.tcj/educartion/f/web/Trichomoniasis/index.htm

  Trichomoniasis is a sexually transmitted protozoal infection caused by Trichomonas vaginalis. […] In women, T vaginalis is isolated from the vagina, cervix, urethra, bladder, and Bartholin and Skene glands. In men, the organism is isolated from the anterior urethra, external genitalia, prostate, epididymis, and semen. […] The protozoan pathogen causes direct damage to the epithelium, leading to microulcerations. […] The mechanism of action is not well understood; however, it is known that anaerobic organisms preferentially reduce the 5-nitro group and active metabolites likely interact with anaerobic bacterial and protozoal DNA.

• #25 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  Human trichomonosis, infection with Trichomonas vaginalis, is the most common non-viral sexually transmitted disease in the world. The host-parasite interaction and pathophysiological processes of trichomonosis remain incompletely understood. This review focuses on the advancements reached in the area of the pathogenesis of T. vaginalis, especially in the role of the cysteine proteinases. It highlights various approaches made in this field and lists a group of trichomonad cysteine proteinases involved in diverse processes such as invasion of the mucous layer, cytoadherence, cytotoxicity, cytoskeleton disruption of red blood cells, hemolysis, and evasion of the host immune response. […] The exact mechanisms of the pathogenesis have not been clearly elucidated to date. However, the sequencing of the T. vaginalis genome has led to knowledge of new gene families involved in the host pathogenesis, leading to new research to understand the mechanism of the parasites pathogenicity better. Trichomonal cytoadherence to epithelial cells is a critical step in the initiation phase of the infection and subsequent pathogenesis.

• #26 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/abs/2014/01/parasite140008/parasite140008.html

  Human trichomonosis, infection with Trichomonas vaginalis, is the most common non-viral sexually transmitted disease in the world. The host-parasite interaction and pathophysiological processes of trichomonosis remain incompletely understood. This review focuses on the advancements reached in the area of the pathogenesis of T. vaginalis, especially in the role of the cysteine proteinases. […] It highlights various approaches made in this field and lists a group of trichomonad cysteine proteinases involved in diverse processes such as invasion of the mucous layer, cytoadherence, cytotoxicity, cytoskeleton disruption of red blood cells, hemolysis, and evasion of the host immune response. A better understanding of the biological roles of cysteine proteinases in the pathogenesis of this parasite could be used in the identification of new chemotherapeutic targets. An additional advantage could be the development of a vaccine in order to reduce transmission of T. vaginalis.

• #27 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  Trichomonad CPs are found in different cell compartments, i.e., lysosomes and plasma membranes, or even released into the culture medium through the lysosome and late/endosomal pathways. In vivo, trichomonad CPs have been found in the vaginal secretions of patients with acute trichomonosis, and some of them are immunogenic. Some CPs have been involved in virulence mechanisms. […] The mucous layer of the genital tract is the first host surface encountered by trichomonads. Mucin, the major proteinaceous constituent of mucous, forms a lattice structure that serves as a formidable physical barrier to microbial invasion. Binding the parasite to mucin followed by its proteolytic degradation by mucinase appears to be the major mechanism by which T. vaginalis can gain access to the underlying epithelium.

• #28 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  Trichomonad CPs are found in different cell compartments, i.e., lysosomes and plasma membranes, or even released into the culture medium through the lysosome and late/endosomal pathways. In vivo, trichomonad CPs have been found in the vaginal secretions of patients with acute trichomonosis, and some of them are immunogenic. Some CPs have been involved in virulence mechanisms. […] The mucous layer of the genital tract is the first host surface encountered by trichomonads. Mucin, the major proteinaceous constituent of mucous, forms a lattice structure that serves as a formidable physical barrier to microbial invasion. Binding the parasite to mucin followed by its proteolytic degradation by mucinase appears to be the major mechanism by which T. vaginalis can gain access to the underlying epithelium.

• #29 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  The adherence mechanism to mucin may allow trichomonads to gain a temporary foothold before penetration into the mucous layer and ultimate parasitism of the underlying epithelial cells. Adherence to host surfaces has been shown to be an early and critical step in Trichomonas pathogenesis. […] The parasites cysteine proteolytic activity is necessary for recognition and adhesion of the parasite to the epithelial cells of the host. […] The protease inhibitors N–p-tosyl-L-lysine-chloromethyl ketone HCl (TLCK) and leupeptin were found to significantly reduce parasite to cervical adenocarcinoma (HeLa) cells and vaginal epithelial cells. […] The numerous CPs synthesized by T. vaginalis contribute significantly to immune evasion. The parasites ability to evade the host immune system is an important aspect of the pathogenesis. Avoidance of complement is used by T. vaginalis to overcome the human immune system. […] Cysteine proteinases are key proteins in the metabolic process; the knowledge of the roles of some CPs in the onset of the infection are very important; it will be useful in order to develop targeted intervention strategies such as vaccines and drugs.

• #30 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  Trichomonad CPs are found in different cell compartments, i.e., lysosomes and plasma membranes, or even released into the culture medium through the lysosome and late/endosomal pathways. In vivo, trichomonad CPs have been found in the vaginal secretions of patients with acute trichomonosis, and some of them are immunogenic. Some CPs have been involved in virulence mechanisms. […] The mucous layer of the genital tract is the first host surface encountered by trichomonads. Mucin, the major proteinaceous constituent of mucous, forms a lattice structure that serves as a formidable physical barrier to microbial invasion. Binding the parasite to mucin followed by its proteolytic degradation by mucinase appears to be the major mechanism by which T. vaginalis can gain access to the underlying epithelium.

• #31 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  The adherence mechanism to mucin may allow trichomonads to gain a temporary foothold before penetration into the mucous layer and ultimate parasitism of the underlying epithelial cells. Adherence to host surfaces has been shown to be an early and critical step in Trichomonas pathogenesis. […] The parasites cysteine proteolytic activity is necessary for recognition and adhesion of the parasite to the epithelial cells of the host. […] The protease inhibitors N–p-tosyl-L-lysine-chloromethyl ketone HCl (TLCK) and leupeptin were found to significantly reduce parasite to cervical adenocarcinoma (HeLa) cells and vaginal epithelial cells. […] The numerous CPs synthesized by T. vaginalis contribute significantly to immune evasion. The parasites ability to evade the host immune system is an important aspect of the pathogenesis. Avoidance of complement is used by T. vaginalis to overcome the human immune system. […] Cysteine proteinases are key proteins in the metabolic process; the knowledge of the roles of some CPs in the onset of the infection are very important; it will be useful in order to develop targeted intervention strategies such as vaccines and drugs.

• #32 Biological roles of cysteine proteinases in the pathogenesis of Trichomonas vaginalis | Parasite

  https://www.parasite-journal.org/articles/parasite/full_html/2014/01/parasite140008/parasite140008.html

  The adherence mechanism to mucin may allow trichomonads to gain a temporary foothold before penetration into the mucous layer and ultimate parasitism of the underlying epithelial cells. Adherence to host surfaces has been shown to be an early and critical step in Trichomonas pathogenesis. […] The parasites cysteine proteolytic activity is necessary for recognition and adhesion of the parasite to the epithelial cells of the host. […] The protease inhibitors N–p-tosyl-L-lysine-chloromethyl ketone HCl (TLCK) and leupeptin were found to significantly reduce parasite to cervical adenocarcinoma (HeLa) cells and vaginal epithelial cells. […] The numerous CPs synthesized by T. vaginalis contribute significantly to immune evasion. The parasites ability to evade the host immune system is an important aspect of the pathogenesis. Avoidance of complement is used by T. vaginalis to overcome the human immune system. […] Cysteine proteinases are key proteins in the metabolic process; the knowledge of the roles of some CPs in the onset of the infection are very important; it will be useful in order to develop targeted intervention strategies such as vaccines and drugs.

• #33 KoreaMed Synapse

  https://synapse.koreamed.org/articles/1044052

  Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. […] We investigated that trichomonads in the vagina sometime after an acute infection secrete proteins like excretory-secretory product that have a chemotactic effect on neutrophils, and that these neutrophils are further stimulated by T. vaginalis to produce chemokines like IL-8 and GRO-, which further promote neutrophil recruitment and chemotaxis. Thus, neutrophil accumulation is believed to maintain or aggravate inflammation. […] However, enhanced neutrophil apoptosis induced by live T. vaginalis could contribute to resolution of inflammation via anti-inflammatory cytokine produced by human macrophage phagocytosed of apoptotic neutrophils. Macrophages may constitute an important component of host defense against T. vaginalis infection, and may be involved in inflammation via production of proinflammatory cytokines and nitric oxide. […] In the host, T. vaginalis uses a capping phenomenon and cleave host immunoglobulins with proteinases as the evasion methods from host immune responses. […] The mechanisms and molecules involved in cytoadherence and pathogenesis of T. vaginalis.

• #34 Trichomonas vaginalis: Pathogenesis, Symbiont Interactions, and Host Cell Immune Responses – PubMed

  https://pubmed.ncbi.nlm.nih.gov/30056833/

  The parasite Trichomonas vaginalis (Tv) causes a highly prevalent sexually transmitted infection. As an extracellular pathogen, the parasite mediates adherence to epithelial cells to colonize the human host. […] Modes of Tv pathogenesis include damage to host tissue mediated by parasite killing of host cells, disruption of steady-state vaginal microbial ecology, and eliciting inflammation by activating the host immune response. […] Mechanisms that may lead to parasite recognition and killing, or the evasion of host immune cells, have also been revealed.

• #35 Trichomoniasis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK534826/

  Trichomonas is a motile organism with a size comparable to a white blood cell. It has at least 4 flagella that provide undulating motility. The organism resides in the lumen of the urogenital tract. The organism releases cytotoxic proteins that destroy the epithelial lining. During an infection, the vaginal pH usually increases. […] In women, T. vaginalis has an incubation period of five to twenty-eight days. Women with trichomoniasis often complain of a foul-smelling yellow or green vaginal discharge, dyspareunia, urinary frequency, dysuria, and/or vulvar pruritus or erythema. In men, it often does not cause symptoms. If a male is symptomatic, the most common symptom is urethritis. Less commonly, men may also develop prostatitis and epididymitis.

• #36

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  On the other hand, the hemolytic activity of the parasite appears to be correlated with virulence. […] The contact-dependent mechanisms described above play an important role in the pathogenesis of the disease. […] There are reports of other parasite products, described as cell-detaching factors (CDF), that are released by the parasite and are known to have trypsin-like activity. […] The rise of vaginal pH during trichomoniasis may therefore be crucial in the pathogenesis of the disease. […] The relationship between protective lactobacilli and T. vaginalis is not completely understood. […] T. vaginalis has numerous ways of evading the immune system, which include evasion of complement-mediated destruction, molecular mimicry, and the ability to coat itself with host plasma proteins.

• #37 Trichomonas vaginalis – Wikipedia

  https://en.wikipedia.org/wiki/Trichomonas_vaginalis

  T. vaginalis causes a very common sexually transmitted disease by sticking to vaginal epithelial cells and breaking them down. It feeds off the host cells and evades the immune system. It secretes extracellular vesicles that disrupt immune function and increase adhesion. Some strains of T. vaginalis stick and kill better than others. Some strains have intracellular viruses or bacteria within them that worsen infections. The parasite also disrupts the healthy balance of bacteria in the vagina. It displaces beneficial ones such as lactobacillus and makes other undesirable bugs more prone to taking its place. Your immune system counterattacks, using things like neutrophils. Neutrophils chew the parasite to death. But T. vaginalis kills immune cells, produces anti-inflammatory signals, and even becomes invisible in clumps to avoid being destroyed.

• #38

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  On the other hand, the hemolytic activity of the parasite appears to be correlated with virulence. […] The contact-dependent mechanisms described above play an important role in the pathogenesis of the disease. […] There are reports of other parasite products, described as cell-detaching factors (CDF), that are released by the parasite and are known to have trypsin-like activity. […] The rise of vaginal pH during trichomoniasis may therefore be crucial in the pathogenesis of the disease. […] The relationship between protective lactobacilli and T. vaginalis is not completely understood. […] T. vaginalis has numerous ways of evading the immune system, which include evasion of complement-mediated destruction, molecular mimicry, and the ability to coat itself with host plasma proteins.

• #39 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  T vaginalis destroys epithelial cells by direct cell contact and by the release of cytotoxic substances. […] It also binds to host plasma proteins, thereby preventing recognition of the parasite by the alternative complement pathway and host proteinases. During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs are the predominant host defense mechanism against T vaginalis and respond to chemotactic substances released by trichomonads. […] Despite the immune systems interaction with T vaginalis, infection produces an immunity that is only partially protective at best, and there is little evidence that a healthy immune system prevents infection. […] One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV-infected women.

• #40 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. […] However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. […] The factors considered to be involved in the pathogenicity of T. vaginalis include; the ability of trichomonads to adhere to vaginal epithelial cells (VECs), the cytotoxic effect of the pathogen on host cells, trichomonad proteinase activity, and the ability of trichomonads to produce subcutaneous abscess lesions in mice. […] In terms of the pathogenesis of T. vaginalis, parasite attachment to host cells is a prerequisite for the establishment of infection, as the organism must overcome constant vaginal secretions.

• #41 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  The pathogenesis of T. vaginalis infection has not been fully elucidated although neutrophil infiltration is considered to be primarily responsible for cytologic changes. […] The chemoattractants proposed to be involved in inflammatory response to T. vaginalis include leukotriene B4 and IL-8, both of which are found in the vaginal discharges of symptomatic trichomoniasis patients. […] These results suggest that live T. vaginalis, particularly when adherence is retained, can induce IL-8 production in neutrophils, and that this action may be mediated through NF-B and MAP kinase signaling pathways. […] Based on the above-described study and several earlier studies, we hypothesize that many trichomonads in the vagina, after acute T. vaginalis infection, secrete proteins, including ES product, and that these have a chemotactic effect on neutrophils.

• #42 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  The pathogenesis of T. vaginalis infection has not been fully elucidated although neutrophil infiltration is considered to be primarily responsible for cytologic changes. […] The chemoattractants proposed to be involved in inflammatory response to T. vaginalis include leukotriene B4 and IL-8, both of which are found in the vaginal discharges of symptomatic trichomoniasis patients. […] These results suggest that live T. vaginalis, particularly when adherence is retained, can induce IL-8 production in neutrophils, and that this action may be mediated through NF-B and MAP kinase signaling pathways. […] Based on the above-described study and several earlier studies, we hypothesize that many trichomonads in the vagina, after acute T. vaginalis infection, secrete proteins, including ES product, and that these have a chemotactic effect on neutrophils.

• #43 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  Moreover, the involvement of vaginal epithelial cells during early infection might promote IL-8 production, and finally, neutrophil accumulation is believed to cause continued inflammation and/or aggravate vaginal inflammation. […] These results indicate that T. vaginalis alters Mcl-1 expression and caspase-3 activation, and thereby, induces the apoptosis of human neutrophils, which strongly suggests that increased neutrophil apoptosis by T. vaginalis contributes to the resolution of inflammation.

• #44 :: Parasites, Hosts and Diseases

  https://www.parahostdis.org/m/journal/view.php?number=270

  Moreover, the involvement of vaginal epithelial cells during early infection might promote IL-8 production, and finally, neutrophil accumulation is believed to cause continued inflammation and/or aggravate vaginal inflammation. […] These results indicate that T. vaginalis alters Mcl-1 expression and caspase-3 activation, and thereby, induces the apoptosis of human neutrophils, which strongly suggests that increased neutrophil apoptosis by T. vaginalis contributes to the resolution of inflammation.

• #45 Infinity war: Trichomonas vaginalis and interactions with host immune response

  https://microbialcell.com/researcharticles/2023a-bongiorni-galego-microbial-cell/

  The transient receptor potential-like channel of T. vaginalis (TvTRPV), cysteine peptidase, and -actinin are currently cited as candidate targets for vaccine development. In this context, the understanding of mechanisms involved in the host-T. vaginalis interaction that elicit the immune response may contribute to the development of new targets to combat trichomoniasis. […] The pathogen-neutrophil interaction goes beyond cytokine production. This in vitro direct contact decreases the myeloid cell leukemia 1 (Mcl-1) expression, an anti-apoptotic protein previously associated with PMNs survival, and increases caspase-3 expression, a protein related to spontaneous apoptosis in neutrophils that triggers the acceleration of the apoptosis process. […] Interestingly, while live trophozoites enhanced the rate of neutrophil apoptosis, trichomonads lysate reduced it.

• #46 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  T vaginalis destroys epithelial cells by direct cell contact and by the release of cytotoxic substances. […] It also binds to host plasma proteins, thereby preventing recognition of the parasite by the alternative complement pathway and host proteinases. During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs are the predominant host defense mechanism against T vaginalis and respond to chemotactic substances released by trichomonads. […] Despite the immune systems interaction with T vaginalis, infection produces an immunity that is only partially protective at best, and there is little evidence that a healthy immune system prevents infection. […] One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV-infected women.

• #47

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  On the other hand, the hemolytic activity of the parasite appears to be correlated with virulence. […] The contact-dependent mechanisms described above play an important role in the pathogenesis of the disease. […] There are reports of other parasite products, described as cell-detaching factors (CDF), that are released by the parasite and are known to have trypsin-like activity. […] The rise of vaginal pH during trichomoniasis may therefore be crucial in the pathogenesis of the disease. […] The relationship between protective lactobacilli and T. vaginalis is not completely understood. […] T. vaginalis has numerous ways of evading the immune system, which include evasion of complement-mediated destruction, molecular mimicry, and the ability to coat itself with host plasma proteins.

• #48 Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

  https://microbialcell.com/researcharticles/trichomoniasis-are-we-giving-the-deserved-attention-to-the-most-common-non-viral-sexually-transmitted-disease-worldwide/

  The second class of T. vaginalis proteins related to adherence comprises the named adhesins five proteins (AP120, AP65, AP51, AP33, and AP23) that apart from AP23, are abundant metabolic enzymes primarily involved in carbohydrate metabolism and found in the hydrogenosome. […] Another important factor contributing to T. vaginalis pathogenesis is the high cytotoxic potential of the parasite. Its ability to promote cytolysis followed by phagocytosis is what triggers the disruption of cell monolayers. […] The host defense in response to T. vaginalis infection involves multiple mechanisms such as non-immunological factors, non-specific and specific mechanisms of the innate immune response. […] Despite all the immune responses mediated by the host cells, T. vaginalis is able to evade those mechanisms and displays the whole pathogenic potential which turns trichomoniasis a chronic and persistent infection.

• #49

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  On the other hand, the hemolytic activity of the parasite appears to be correlated with virulence. […] The contact-dependent mechanisms described above play an important role in the pathogenesis of the disease. […] There are reports of other parasite products, described as cell-detaching factors (CDF), that are released by the parasite and are known to have trypsin-like activity. […] The rise of vaginal pH during trichomoniasis may therefore be crucial in the pathogenesis of the disease. […] The relationship between protective lactobacilli and T. vaginalis is not completely understood. […] T. vaginalis has numerous ways of evading the immune system, which include evasion of complement-mediated destruction, molecular mimicry, and the ability to coat itself with host plasma proteins.

• #50 Cited

  https://www.koreamed.org/SearchBasic.php?RID=1720505

  However, enhanced neutrophil apoptosis induced by live T. vaginalis could contribute to resolution of inflammation. […] Macrophages may constitute an important component of host defense against T. vaginalis infection. […] In the host, T. vaginalis uses a capping phenomenon to cleave host immunoglobulins with proteinases and thus escape from host immune responses.

• #51 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  T vaginalis destroys epithelial cells by direct cell contact and by the release of cytotoxic substances. […] It also binds to host plasma proteins, thereby preventing recognition of the parasite by the alternative complement pathway and host proteinases. During infection, the vaginal pH increases, as does the number of polymorphonuclear leukocytes (PMNs). PMNs are the predominant host defense mechanism against T vaginalis and respond to chemotactic substances released by trichomonads. […] Despite the immune systems interaction with T vaginalis, infection produces an immunity that is only partially protective at best, and there is little evidence that a healthy immune system prevents infection. […] One study showed no association between trichomoniasis and the use of protease inhibitors or immune status in HIV-infected women.

• #52 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-is-Trichomoniasis.aspx

  In addition, the parasite has the propensity to adsorb host plasma proteins that have a role in its protection or nutrition or protection. The production of extracellular proteases (most notably, cysteine proteases) may represent a potential virulence factor by inactivating or altering a plethora of host proteins. […] Clearly, trichomoniasis has been acknowledged in the recent decades as being more important condition than previously thought. Some important questions remain regarding the immunology of the pathogen, potential complications in pregnancy, achieving accurate diagnosis, as well as public health control of this parasite and the infection it causes.

• #53 KoreaMed Synapse

  https://synapse.koreamed.org/articles/1044052

  Vaginal trichomoniasis, caused by Trichomonas vaginalis, is the most common sexually transmitted disease. However, despite its high prevalence, the pathogenesis of T. vaginalis infection has not been clearly characterized although neutrophil infiltration is considered to be primarily responsible for the cytologic changes associated with this infection. […] We investigated that trichomonads in the vagina sometime after an acute infection secrete proteins like excretory-secretory product that have a chemotactic effect on neutrophils, and that these neutrophils are further stimulated by T. vaginalis to produce chemokines like IL-8 and GRO-, which further promote neutrophil recruitment and chemotaxis. Thus, neutrophil accumulation is believed to maintain or aggravate inflammation. […] However, enhanced neutrophil apoptosis induced by live T. vaginalis could contribute to resolution of inflammation via anti-inflammatory cytokine produced by human macrophage phagocytosed of apoptotic neutrophils. Macrophages may constitute an important component of host defense against T. vaginalis infection, and may be involved in inflammation via production of proinflammatory cytokines and nitric oxide. […] In the host, T. vaginalis uses a capping phenomenon and cleave host immunoglobulins with proteinases as the evasion methods from host immune responses. […] The mechanisms and molecules involved in cytoadherence and pathogenesis of T. vaginalis.

• #54 Trichomonas vaginalis – Wikipedia

  https://en.wikipedia.org/wiki/Trichomonas_vaginalis

  T. vaginalis causes a very common sexually transmitted disease by sticking to vaginal epithelial cells and breaking them down. It feeds off the host cells and evades the immune system. It secretes extracellular vesicles that disrupt immune function and increase adhesion. Some strains of T. vaginalis stick and kill better than others. Some strains have intracellular viruses or bacteria within them that worsen infections. The parasite also disrupts the healthy balance of bacteria in the vagina. It displaces beneficial ones such as lactobacillus and makes other undesirable bugs more prone to taking its place. Your immune system counterattacks, using things like neutrophils. Neutrophils chew the parasite to death. But T. vaginalis kills immune cells, produces anti-inflammatory signals, and even becomes invisible in clumps to avoid being destroyed.

• #55 Trichomonas vaginalis – Wikipedia

  https://en.wikipedia.org/wiki/Trichomonas_vaginalis

  T. vaginalis causes a very common sexually transmitted disease by sticking to vaginal epithelial cells and breaking them down. It feeds off the host cells and evades the immune system. It secretes extracellular vesicles that disrupt immune function and increase adhesion. Some strains of T. vaginalis stick and kill better than others. Some strains have intracellular viruses or bacteria within them that worsen infections. The parasite also disrupts the healthy balance of bacteria in the vagina. It displaces beneficial ones such as lactobacillus and makes other undesirable bugs more prone to taking its place. Your immune system counterattacks, using things like neutrophils. Neutrophils chew the parasite to death. But T. vaginalis kills immune cells, produces anti-inflammatory signals, and even becomes invisible in clumps to avoid being destroyed.

• #56 Trichomonas vaginalis – Wikipedia

  https://en.wikipedia.org/wiki/Trichomonas_vaginalis

  T. vaginalis causes a very common sexually transmitted disease by sticking to vaginal epithelial cells and breaking them down. It feeds off the host cells and evades the immune system. It secretes extracellular vesicles that disrupt immune function and increase adhesion. Some strains of T. vaginalis stick and kill better than others. Some strains have intracellular viruses or bacteria within them that worsen infections. The parasite also disrupts the healthy balance of bacteria in the vagina. It displaces beneficial ones such as lactobacillus and makes other undesirable bugs more prone to taking its place. Your immune system counterattacks, using things like neutrophils. Neutrophils chew the parasite to death. But T. vaginalis kills immune cells, produces anti-inflammatory signals, and even becomes invisible in clumps to avoid being destroyed.

• #57 Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis | PLOS Neglected Tropical Diseases

  https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011693

  Finally, we show that co-inoculation of T. vaginalis extracellular vesicles (TvEVs) and parasites results in higher parasite burden in vivo. […] To establish infection, Tv adheres to the epithelial lining of the urogenital tract by transitioning from a free-swimming ovoid cell into its adherent amoeboid form. […] It is thought that the level of parasite binding to host cells seen in vitro mimics the outcome of infection in vivo, but this has correlation has yet to be investigated. […] Here we have established an in vivo T. vaginalis pathogenesis model using the male mouse urogenital tract (MUT). […] Using this model, we demonstrate that Tv strains which are more adherent to host cells in vitro result in higher parasite burden in vivo, providing the first direct evidence that parasite adherence to host cells affects the ability of the parasite to establish infection in vivo.

• #58 Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis | PLOS Neglected Tropical Diseases

  https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011693

  We also established a correlation between the ability of parasite secreted EVs to increase the adherence of Tv to host cell monolayers in vitro and increased survival of the parasite in our murine model. […] These data illustrate for the first time that TvEVs play a role in host:parasite interactions in vivo and confirm previous in vitro-based predictions that TvEVs assist the parasite in colonizing the host in vivo.

• #59 Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis | PLOS Neglected Tropical Diseases

  https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011693

  Finally, we show that co-inoculation of T. vaginalis extracellular vesicles (TvEVs) and parasites results in higher parasite burden in vivo. […] To establish infection, Tv adheres to the epithelial lining of the urogenital tract by transitioning from a free-swimming ovoid cell into its adherent amoeboid form. […] It is thought that the level of parasite binding to host cells seen in vitro mimics the outcome of infection in vivo, but this has correlation has yet to be investigated. […] Here we have established an in vivo T. vaginalis pathogenesis model using the male mouse urogenital tract (MUT). […] Using this model, we demonstrate that Tv strains which are more adherent to host cells in vitro result in higher parasite burden in vivo, providing the first direct evidence that parasite adherence to host cells affects the ability of the parasite to establish infection in vivo.

• #60 Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis | PLOS Neglected Tropical Diseases

  https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011693

  We also established a correlation between the ability of parasite secreted EVs to increase the adherence of Tv to host cell monolayers in vitro and increased survival of the parasite in our murine model. […] These data illustrate for the first time that TvEVs play a role in host:parasite interactions in vivo and confirm previous in vitro-based predictions that TvEVs assist the parasite in colonizing the host in vivo.

• #61 Trichomonas vaginalis adherence phenotypes and extracellular vesicles impact parasite survival in a novel in vivo model of pathogenesis | PLOS Neglected Tropical Diseases

  https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011693

  We also established a correlation between the ability of parasite secreted EVs to increase the adherence of Tv to host cell monolayers in vitro and increased survival of the parasite in our murine model. […] These data illustrate for the first time that TvEVs play a role in host:parasite interactions in vivo and confirm previous in vitro-based predictions that TvEVs assist the parasite in colonizing the host in vivo.

• #62 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  T. vaginalis is a parasitic pathogen primarily infecting squamous epithelial cells of the human genital tract, causing damage to these cells. […] It has its own microbiota, harboring two Mycoplasma species and a double-stranded RNA virus, T. vaginalis virus (TVV), which can contribute to its pathogenesis. […] TVV2 and TVV3 to surface expression of an immunogenic protein, P270, which is associated with cytotoxicity, cytoadherence, and host immune evasion. […] The greater likelihood of persistence in women is linked to greater availability of iron, an essential nutrient. […] Menstrual blood creates a rich growth medium which promotes attachment and growth of the parasite in the vaginal canal. […] The physiological mechanisms linking T. vaginalis and adverse birth outcomes are not well understood. One hypothesis is that PTD and PROM in T. vaginalis-infected pregnant women are related to maternal innate immune inflammatory responses to the parasite, which involve elevated cervical interleukin-8 (IL-8) and vaginal defensin levels.

• #63

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  The roles played by pH and hormones in trichomoniasis may explain the observation that the symptoms of the disease are often worse during menstruation. […] The presence of double-stranded RNA (dsRNA) viruses (T. vaginalis RNA virus; TVV) in trichomoniasis was found to correlate with variation of the expression of certain surface antigens, and loss of the dsRNA accompanied loss of antigen expression. […] However, the precise role of dsRNA viruses in the pathogenesis of trichomoniasis remains to be determined. […] Experimental studies have shown that female animals are more susceptible to infection than their male counterparts. […] The oxidative nature of the male genital tract is hypothesized to be inhibitory to certain pathogenic factors of the protozoan. […] In contrast, the vagina is a reducing environment, which may contribute to the activation of some pathogenic mechanisms of T. vaginalis. […] Further, for understanding the strain differences in the virulence of the parasite, there are no well-documented physical or biochemical determinants of virulence factors on the basis of which strains can be classified.

• #64

  https://journals.lww.com/ijst/fulltext/2008/29010/an_update_on_trichomonas_vaginalis.2.aspx

  The roles played by pH and hormones in trichomoniasis may explain the observation that the symptoms of the disease are often worse during menstruation. […] The presence of double-stranded RNA (dsRNA) viruses (T. vaginalis RNA virus; TVV) in trichomoniasis was found to correlate with variation of the expression of certain surface antigens, and loss of the dsRNA accompanied loss of antigen expression. […] However, the precise role of dsRNA viruses in the pathogenesis of trichomoniasis remains to be determined. […] Experimental studies have shown that female animals are more susceptible to infection than their male counterparts. […] The oxidative nature of the male genital tract is hypothesized to be inhibitory to certain pathogenic factors of the protozoan. […] In contrast, the vagina is a reducing environment, which may contribute to the activation of some pathogenic mechanisms of T. vaginalis. […] Further, for understanding the strain differences in the virulence of the parasite, there are no well-documented physical or biochemical determinants of virulence factors on the basis of which strains can be classified.

• #65 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  T. vaginalis is a parasitic pathogen primarily infecting squamous epithelial cells of the human genital tract, causing damage to these cells. […] It has its own microbiota, harboring two Mycoplasma species and a double-stranded RNA virus, T. vaginalis virus (TVV), which can contribute to its pathogenesis. […] TVV2 and TVV3 to surface expression of an immunogenic protein, P270, which is associated with cytotoxicity, cytoadherence, and host immune evasion. […] The greater likelihood of persistence in women is linked to greater availability of iron, an essential nutrient. […] Menstrual blood creates a rich growth medium which promotes attachment and growth of the parasite in the vaginal canal. […] The physiological mechanisms linking T. vaginalis and adverse birth outcomes are not well understood. One hypothesis is that PTD and PROM in T. vaginalis-infected pregnant women are related to maternal innate immune inflammatory responses to the parasite, which involve elevated cervical interleukin-8 (IL-8) and vaginal defensin levels.

• #66 Management and control of Trichomonas vaginalis infection – Das – Annals of Infection

  https://aoi.amegroups.org/article/view/5006/html

  TV infection is invariably associated with both other sexually transmitted infections (STIs) as well as several non-STIs. […] Influence of other vaginal coinfections on the management of TV with metronidazole therapy is not clearly known. […] M. hominis-infected TV strains showed higher minimum inhibitory concentration (MIC) to metronidazole than the respective non-infected strains. […] Considering the inhibitory influence of coinfections in the metronidazole therapy for TV infection, a seven-day therapy appears appropriate. […] In spite of reasonable susceptibility of metronidazole against TV, the high rate of test of cure positives in the recent RCT, even among those receiving multidose metronidazole, requires search for more efficacious low-cost treatments for trichomoniasis.

• #67 Infinity war: Trichomonas vaginalis and interactions with host immune response

  https://microbialcell.com/researcharticles/2023a-bongiorni-galego-microbial-cell/

  Infection with T. vaginalis increased the risk of acquiring HIV by 1.5 times compared to uninfected individuals. […] The symbiosis between T. vaginalis and M. hominis may play a role in the clinical worsening observed in trichomoniasis during pregnancy. […] The association between T. vaginalis and prostate cancer is debatable. […] The long permanence of T. vaginalis may cause several clinical complications. Three of them are highlighted: the increase in HIV transmission and acquisition due to the disruption of the mucosal barrier, reduction of SLPI, and recruitment of CD4+T cells; adverse pregnancy outcomes caused by a systemic inflammatory response with cytokine production, neutrophil migration, and M. hominis release into the extracellular environment; and prostate cancer attributed to a sequence of inflammatory mechanisms that increased the invasiveness and growth of prostate cells, creating a perfect microenvironment for the establishment of cancer.

• #68 Trichomoniasis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/trichomoniasis/symptoms-causes/syc-20378609

  Trichomoniasis is caused by a one-celled protozoan, a type of tiny parasite called Trichomonas vaginalis. The parasite passes between people during genital contact, including vaginal, oral or anal sex. The infection can be passed between men and women, women, and sometimes men. […] The parasite infects the lower genital tract. In women, this includes the outer part of the genitals (vulva), vagina, opening of the uterus (cervix) and the urinary opening (urethra). In men, the parasite infects the inside of the penis (urethra). […] Having trichomoniasis causes irritation in the genital area that may make it easier for other sexually transmitted infections (STIs) to enter the body or to pass them to others. Trichomoniasis also appears to make it easier to become infected with human immunodeficiency virus (HIV), the virus that causes acquired immunodeficiency syndrome (AIDS). […] Trichomoniasis is associated with an increased risk of cervical or prostate cancer. […] Untreated, trichomoniasis infection can last for months to years.

• #69

  https://www.who.int/news-room/fact-sheets/detail/trichomoniasis

  Trichomonas vaginalis is a preventable and curable sexually transmitted protozoan that infects the urogenital tract. […] Infection with T. vaginalis is also associated with increased risk of HIV acquisition. […] Untreated T. vaginalis is linked to adverse birth outcomes, including low birth weight, preterm delivery and premature rupture of membranes. […] T. vaginalis infections are linked to a 1.5 times increased risk of HIV acquisition. […] Although antimicrobial resistance in T. vaginalis is not widespread, WHO closely monitors patterns of potential antimicrobial resistance of this pathogen to inform treatment recommendations and national policies. […] In 2024, WHO published Recommendations for the treatment of Trichomonas vaginalis, Mycoplasma genitalium, Candida albicans, bacterial vaginosis and human papillomavirus (anogenital warts) to provide evidence-informed clinical and practical recommendations on case management of Trichomonas vaginalis.

• #70 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  The greater susceptibility to HIV among T. vaginalis-infected individuals is plausible for several reasons: (1) T. vaginalis damages host epithelial cell membranes which act as a structural barrier to HIV, (2) the host immune response to T. vaginalis stimulates an increased number of HIV target cells in the genital tract mucosa, and (3) T. vaginalis alters the normal vaginal microbiota, rendering it more permissive to the development of BV, which, in turn, increases HIV acquisition risk. […] T. vaginalis is not traditionally considered an STI associated with pelvic inflammatory disease (PID). However, in an older study of 119 South African women, those infected with T. vaginalis had a significantly higher risk of PID than those without. […] This is thought to be due to inflammatory damage of female reproductive organs and changes in the vaginal environment resulting in decrease or loss of reproductive function in women. […] While thought to be a vaginal infection, there is some evidence to suggest that T. vaginalis causes cervical involvement.

• #71 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  Another showed that HIV seropositivity did not alter the rate of infection in males. […] T vaginalis infection has even been shown to increase a patients susceptibility to sexually transmitted viruses, including herpes simplex virus, human papillomavirus, and HIV. […] One potential explanation for this is that T vaginalis disrupts the epithelial monolayer, leading to increased passage of the HIV virus. […] Another posits that T vaginalis induces immune activation, specifically lymphocyte activation and replication and cytokine production, leading to increased viral replication in HIV-infected cells. Further research is needed to clarify the exact mechanism by which T vaginalis increases the risk for HIV infection.

• #72 Trichomoniasis: Background, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/230617-overview

  Another showed that HIV seropositivity did not alter the rate of infection in males. […] T vaginalis infection has even been shown to increase a patients susceptibility to sexually transmitted viruses, including herpes simplex virus, human papillomavirus, and HIV. […] One potential explanation for this is that T vaginalis disrupts the epithelial monolayer, leading to increased passage of the HIV virus. […] Another posits that T vaginalis induces immune activation, specifically lymphocyte activation and replication and cytokine production, leading to increased viral replication in HIV-infected cells. Further research is needed to clarify the exact mechanism by which T vaginalis increases the risk for HIV infection.

• #73 Trichomoniasis – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/trichomoniasis/symptoms-causes/syc-20378609

  Trichomoniasis is caused by a one-celled protozoan, a type of tiny parasite called Trichomonas vaginalis. The parasite passes between people during genital contact, including vaginal, oral or anal sex. The infection can be passed between men and women, women, and sometimes men. […] The parasite infects the lower genital tract. In women, this includes the outer part of the genitals (vulva), vagina, opening of the uterus (cervix) and the urinary opening (urethra). In men, the parasite infects the inside of the penis (urethra). […] Having trichomoniasis causes irritation in the genital area that may make it easier for other sexually transmitted infections (STIs) to enter the body or to pass them to others. Trichomoniasis also appears to make it easier to become infected with human immunodeficiency virus (HIV), the virus that causes acquired immunodeficiency syndrome (AIDS). […] Trichomoniasis is associated with an increased risk of cervical or prostate cancer. […] Untreated, trichomoniasis infection can last for months to years.

• #74 Researchers discover mechanism leading from trichomoniasis to prostate cancer – ecancer

  https://ecancer.org/en/news/3337-researchers-discover-mechanism-leading-from-trichomoniasis-to-prostate-cancer

  Researchers discover mechanism leading from trichomoniasis to prostate cancer. Researchers have identified a way in which men can develop prostate cancer after contracting trichomoniasis, a curable but often overlooked sexually transmitted disease. Previous studies have teased out a casual, epidemiological correlation between the two diseases, but this latest study suggests a more tangible biological mechanism. John Alderete, a professor at Washington State University’s School of Molecular Biosciences, says the trichomoniasis parasite activates a suite of proteins, the last of which makes sure the proteins stay active. This latest study, she says, „is providing a molecular mechanism that might explain that association.” WSU cancer researcher Nancy Magnuson is an expert on the protein PIM1, a promoter of cancer cell growth, and identified the protein in the cascade of proteins leading from trichomoniasis to prostate cancer. WSU molecular biologist Ray Reeves brought to bear his expertise in HMGA1. The protein turns genes on and off and ended up being the actor making sure other proteins in the trichomoniasis-to-cancer sequence stay on. Alderete hopes knowledge of the mechanism will lead to better diagnosis and treatment.

• #75 Mechanism leading from trichomoniasis to prostate cancer identified | ScienceDaily

  https://www.sciencedaily.com/releases/2012/08/120830065821.htm

  Researchers have identified a way in which men can develop prostate cancer after contracting trichomoniasis, a curable but often overlooked sexually transmitted disease. […] Previous studies have teased out a casual, epidemiological correlation between the two diseases, but this latest study suggests a more tangible biological mechanism. […] John Alderete, a professor at Washington State University’s School of Molecular Biosciences, says the trichomoniasis parasite activates a suite of proteins, the last of which makes sure the proteins stay active. […] Infected men have a 40 percent greater chance of developing prostate cancer, according to a 2006 study led by Siobhan Sutcliffe, a Washington University epidemiologist and co-author of the recent PLoS Pathogens paper. […] This latest study, she says, „is providing a molecular mechanism that might explain that association.”

• #76 Mechanism leading from trichomoniasis to prostate cancer identified | ScienceDaily

  https://www.sciencedaily.com/releases/2012/08/120830065821.htm

  Researchers have identified a way in which men can develop prostate cancer after contracting trichomoniasis, a curable but often overlooked sexually transmitted disease. […] Previous studies have teased out a casual, epidemiological correlation between the two diseases, but this latest study suggests a more tangible biological mechanism. […] John Alderete, a professor at Washington State University’s School of Molecular Biosciences, says the trichomoniasis parasite activates a suite of proteins, the last of which makes sure the proteins stay active. […] Infected men have a 40 percent greater chance of developing prostate cancer, according to a 2006 study led by Siobhan Sutcliffe, a Washington University epidemiologist and co-author of the recent PLoS Pathogens paper. […] This latest study, she says, „is providing a molecular mechanism that might explain that association.”

• #77 Mechanism leading from trichomoniasis to prostate cancer identified | ScienceDaily

  https://www.sciencedaily.com/releases/2012/08/120830065821.htm

  WSU cancer researcher Nancy Magnuson is an expert on the protein PIM1, a promoter of cancer cell growth, and identified the protein in the cascade of proteins leading from trichomoniasis to prostate cancer. […] The protein turns genes on and off and ended up being the actor making sure other proteins in the trichomoniasis-to-cancer sequence stay on. […] Alderete hopes knowledge of the mechanism will lead to better diagnosis and treatment.

• #78 Association between trichomoniasis and prostate and bladder diseases: a population-based case–control study | Scientific Reports

  https://www.nature.com/articles/s41598-022-19561-2

  Trichomonas vaginalis infection is one of the most widespread sexually transmitted infections in the world. The chronic inflammation induced by persistent infection may increase the risk of developing genitourinary cancers. […] Trichomoniasis exposure had a significant association with BPH and PCa (adjusted OR: BPH=2.685, 95% CI=1.2334.286, P=0.013; PCa=5.801, 95% CI=1.29626.035, P=0.016). […] The mechanism of T. vaginalis inducing BPH and PCa still remains unclear. Several studies have demonstrated different possible mechanisms. In women, T. vaginalis induces pro-inflammatory cytokine production, including interleukin-6 (IL-6), interleukin-8 (IL-8), and chemokine ligand 2 (CCL2), while attaching to vaginal epithelial cells. A similar inflammatory reaction was also noted in T. vaginalis-infected prostatic epithelial cells in some in vitro studies. Repeated cell damage and repair in chronic inflammation is likely to play an important role in inducing BPH. Furthermore, the alteration in cytokine expression during chronic inflammation may have effects on cell growth and proliferation of the prostate epithelium and stroma in BPH. The activated mast cells stimulated by T. vaginalis-infected prostatic epithelial cells can initiate IL-8 and CCL2 expression. IL-8 could be a predictive marker for BPH. Some in vitro studies demonstrated that IL-8 can stimulate fibroblast growth factor 2 (FGF-2), which causes the mitosis of prostate stromal cells. IL-8 could also cause cyclin D1 expression to promote stromal cells proliferation. In addition, CCL2, secreted by the prostatic stroma fibroblast, could promote both BPH and PCa progression.

• #79 Association between trichomoniasis and prostate and bladder diseases: a population-based case–control study | Scientific Reports

  https://www.nature.com/articles/s41598-022-19561-2

  T. vaginalis possibly induces carcinogenesis of the prostate. The infected prostatic epithelial cells produce IL-6 in chronic inflammation. In early studies, an elevated serum IL-6 level was noted in patients with advanced PCa. The positive correlation between IL-6 receptor expression and cell proliferation has been reported. IL-6 also induces epithelial-mesenchymal transition (EMT) in breast cancer growth and metastasis, and the same reaction may also occur in prostatic epithelial cells. In addition, more than one study has demonstrated that IL-6 could enhance androgen receptor (AR) activity and AR gene expression, which is also related to prostate cancer growth. […] The joint effect of trichomoniasis and depression could increase the risk of BPH, PCa, or BC.

• #80 Association between trichomoniasis and prostate and bladder diseases: a population-based case–control study | Scientific Reports

  https://www.nature.com/articles/s41598-022-19561-2

  Trichomonas vaginalis infection is one of the most widespread sexually transmitted infections in the world. The chronic inflammation induced by persistent infection may increase the risk of developing genitourinary cancers. […] Trichomoniasis exposure had a significant association with BPH and PCa (adjusted OR: BPH=2.685, 95% CI=1.2334.286, P=0.013; PCa=5.801, 95% CI=1.29626.035, P=0.016). […] The mechanism of T. vaginalis inducing BPH and PCa still remains unclear. Several studies have demonstrated different possible mechanisms. In women, T. vaginalis induces pro-inflammatory cytokine production, including interleukin-6 (IL-6), interleukin-8 (IL-8), and chemokine ligand 2 (CCL2), while attaching to vaginal epithelial cells. A similar inflammatory reaction was also noted in T. vaginalis-infected prostatic epithelial cells in some in vitro studies. Repeated cell damage and repair in chronic inflammation is likely to play an important role in inducing BPH. Furthermore, the alteration in cytokine expression during chronic inflammation may have effects on cell growth and proliferation of the prostate epithelium and stroma in BPH. The activated mast cells stimulated by T. vaginalis-infected prostatic epithelial cells can initiate IL-8 and CCL2 expression. IL-8 could be a predictive marker for BPH. Some in vitro studies demonstrated that IL-8 can stimulate fibroblast growth factor 2 (FGF-2), which causes the mitosis of prostate stromal cells. IL-8 could also cause cyclin D1 expression to promote stromal cells proliferation. In addition, CCL2, secreted by the prostatic stroma fibroblast, could promote both BPH and PCa progression.

• #81

  https://www.who.int/news-room/fact-sheets/detail/trichomoniasis

  Trichomonas vaginalis is a preventable and curable sexually transmitted protozoan that infects the urogenital tract. […] Infection with T. vaginalis is also associated with increased risk of HIV acquisition. […] Untreated T. vaginalis is linked to adverse birth outcomes, including low birth weight, preterm delivery and premature rupture of membranes. […] T. vaginalis infections are linked to a 1.5 times increased risk of HIV acquisition. […] Although antimicrobial resistance in T. vaginalis is not widespread, WHO closely monitors patterns of potential antimicrobial resistance of this pathogen to inform treatment recommendations and national policies. […] In 2024, WHO published Recommendations for the treatment of Trichomonas vaginalis, Mycoplasma genitalium, Candida albicans, bacterial vaginosis and human papillomavirus (anogenital warts) to provide evidence-informed clinical and practical recommendations on case management of Trichomonas vaginalis.

• #82 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  T. vaginalis is a parasitic pathogen primarily infecting squamous epithelial cells of the human genital tract, causing damage to these cells. […] It has its own microbiota, harboring two Mycoplasma species and a double-stranded RNA virus, T. vaginalis virus (TVV), which can contribute to its pathogenesis. […] TVV2 and TVV3 to surface expression of an immunogenic protein, P270, which is associated with cytotoxicity, cytoadherence, and host immune evasion. […] The greater likelihood of persistence in women is linked to greater availability of iron, an essential nutrient. […] Menstrual blood creates a rich growth medium which promotes attachment and growth of the parasite in the vaginal canal. […] The physiological mechanisms linking T. vaginalis and adverse birth outcomes are not well understood. One hypothesis is that PTD and PROM in T. vaginalis-infected pregnant women are related to maternal innate immune inflammatory responses to the parasite, which involve elevated cervical interleukin-8 (IL-8) and vaginal defensin levels.

• #83 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  T. vaginalis is a parasitic pathogen primarily infecting squamous epithelial cells of the human genital tract, causing damage to these cells. […] It has its own microbiota, harboring two Mycoplasma species and a double-stranded RNA virus, T. vaginalis virus (TVV), which can contribute to its pathogenesis. […] TVV2 and TVV3 to surface expression of an immunogenic protein, P270, which is associated with cytotoxicity, cytoadherence, and host immune evasion. […] The greater likelihood of persistence in women is linked to greater availability of iron, an essential nutrient. […] Menstrual blood creates a rich growth medium which promotes attachment and growth of the parasite in the vaginal canal. […] The physiological mechanisms linking T. vaginalis and adverse birth outcomes are not well understood. One hypothesis is that PTD and PROM in T. vaginalis-infected pregnant women are related to maternal innate immune inflammatory responses to the parasite, which involve elevated cervical interleukin-8 (IL-8) and vaginal defensin levels.

• #84 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  The greater susceptibility to HIV among T. vaginalis-infected individuals is plausible for several reasons: (1) T. vaginalis damages host epithelial cell membranes which act as a structural barrier to HIV, (2) the host immune response to T. vaginalis stimulates an increased number of HIV target cells in the genital tract mucosa, and (3) T. vaginalis alters the normal vaginal microbiota, rendering it more permissive to the development of BV, which, in turn, increases HIV acquisition risk. […] T. vaginalis is not traditionally considered an STI associated with pelvic inflammatory disease (PID). However, in an older study of 119 South African women, those infected with T. vaginalis had a significantly higher risk of PID than those without. […] This is thought to be due to inflammatory damage of female reproductive organs and changes in the vaginal environment resulting in decrease or loss of reproductive function in women. […] While thought to be a vaginal infection, there is some evidence to suggest that T. vaginalis causes cervical involvement.

• #85 Trichomoniasis | Article | GLOWM

  https://www.glowm.com/article/heading/vol-12–infections-in-gynecology–trichomoniasis/id/419923

  The greater susceptibility to HIV among T. vaginalis-infected individuals is plausible for several reasons: (1) T. vaginalis damages host epithelial cell membranes which act as a structural barrier to HIV, (2) the host immune response to T. vaginalis stimulates an increased number of HIV target cells in the genital tract mucosa, and (3) T. vaginalis alters the normal vaginal microbiota, rendering it more permissive to the development of BV, which, in turn, increases HIV acquisition risk. […] T. vaginalis is not traditionally considered an STI associated with pelvic inflammatory disease (PID). However, in an older study of 119 South African women, those infected with T. vaginalis had a significantly higher risk of PID than those without. […] This is thought to be due to inflammatory damage of female reproductive organs and changes in the vaginal environment resulting in decrease or loss of reproductive function in women. […] While thought to be a vaginal infection, there is some evidence to suggest that T. vaginalis causes cervical involvement.

• #86 Transcriptional profile of Trichomonas vaginalis in response to metronidazole | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09339-9

  The current study reveals evident nuclear and cytomembrane damage and multiple variations in T. vaginalis at the transcriptional level. […] These data will offer a meaningful foundation for a deeper understanding of the MTZ trichomonacidal process and the transcriptional response of T. vaginalis to MTZ-induced stress or even cell death. […] After decades of unremitting efforts by scientists, research on the mechanism by which MTZ kills T. vaginalis has made tremendous progress, however, it has not yet been fully illustrated. […] As a prodrug, MTZ is inactive until it enters T. vaginalis and becomes activated after its nitro group is reduced to cytotoxic nitro radical anions. […] Previous studies revealed several MTZ activation-related molecules, such as pyruvate:ferredoxin oxidoreductase (PFOR), ferredoxin (Fd) and the flavin enzyme thioredoxin reductase (TrxR).

• #87 Trichomoniasis Treatment & Management: Approach Considerations, Pharmacologic Therapy, Diet and Activity

  https://emedicine.medscape.com/article/230617-treatment

  The mechanism of action for these drugs is not completely understood. It is thought that target organisms preferentially reduce the 5-nitro group on the molecule, creating active metabolites that disrupt the helical structure of DNA. This prevents nucleic acid synthesis and eventually leads to cell death. […] Despite the widespread use of nitroimidazoles in the treatment of trichomoniasis, resistance to these drugs is rare and is typically solved by increasing the dose or switching to another nitroimidazole. The CDC has reported incidents of trichomoniasis resistant to metronidazole that were susceptible to tinidazole. […] When standard treatment regimens fail, a regimen of 2 g of oral metronidazole or tinidazole for 5 days may be considered. Inpatient intravenous (IV) therapy may be indicated when resistance is present.

• #88 Transcriptional profile of Trichomonas vaginalis in response to metronidazole | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09339-9

  The current study reveals evident nuclear and cytomembrane damage and multiple variations in T. vaginalis at the transcriptional level. […] These data will offer a meaningful foundation for a deeper understanding of the MTZ trichomonacidal process and the transcriptional response of T. vaginalis to MTZ-induced stress or even cell death. […] After decades of unremitting efforts by scientists, research on the mechanism by which MTZ kills T. vaginalis has made tremendous progress, however, it has not yet been fully illustrated. […] As a prodrug, MTZ is inactive until it enters T. vaginalis and becomes activated after its nitro group is reduced to cytotoxic nitro radical anions. […] Previous studies revealed several MTZ activation-related molecules, such as pyruvate:ferredoxin oxidoreductase (PFOR), ferredoxin (Fd) and the flavin enzyme thioredoxin reductase (TrxR).

• #89 Transcriptional profile of Trichomonas vaginalis in response to metronidazole | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09339-9

  A previous study concluded that a strong correlation existed between the presence of PFOR activity and MTZ among different microorganisms. […] Therefore, as the key proteins for MTZ activation, the wide downregulation of PFOR was likely to be a self-rescue response at the early stage. […] However, one of three genes mapped to thioredoxin reductase and five of six DEGs encoding nitroreductase family proteins were significantly upregulated by approximately 3.8-to to even 739.3-fold. […] Thioredoxin reductase (with nitroreductase activity) and nitroreductase have been reported to play roles in activating MTZ against T. vaginalis depending on an alternative theory. […] The significantly enriched upregulated genes were mainly involved in the basic life process, similar to the GO analysis.

• #90 Trichomoniasis Treatment & Management: Approach Considerations, Pharmacologic Therapy, Diet and Activity

  https://emedicine.medscape.com/article/230617-treatment

  The mechanism of action for these drugs is not completely understood. It is thought that target organisms preferentially reduce the 5-nitro group on the molecule, creating active metabolites that disrupt the helical structure of DNA. This prevents nucleic acid synthesis and eventually leads to cell death. […] Despite the widespread use of nitroimidazoles in the treatment of trichomoniasis, resistance to these drugs is rare and is typically solved by increasing the dose or switching to another nitroimidazole. The CDC has reported incidents of trichomoniasis resistant to metronidazole that were susceptible to tinidazole. […] When standard treatment regimens fail, a regimen of 2 g of oral metronidazole or tinidazole for 5 days may be considered. Inpatient intravenous (IV) therapy may be indicated when resistance is present.

• #91 Trichomoniasis Treatment & Management: Approach Considerations, Pharmacologic Therapy, Diet and Activity

  https://emedicine.medscape.com/article/230617-treatment

  The mechanism of action for these drugs is not completely understood. It is thought that target organisms preferentially reduce the 5-nitro group on the molecule, creating active metabolites that disrupt the helical structure of DNA. This prevents nucleic acid synthesis and eventually leads to cell death. […] Despite the widespread use of nitroimidazoles in the treatment of trichomoniasis, resistance to these drugs is rare and is typically solved by increasing the dose or switching to another nitroimidazole. The CDC has reported incidents of trichomoniasis resistant to metronidazole that were susceptible to tinidazole. […] When standard treatment regimens fail, a regimen of 2 g of oral metronidazole or tinidazole for 5 days may be considered. Inpatient intravenous (IV) therapy may be indicated when resistance is present.

• #92 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Trichomoniasis is the most common, sexually transmitted infection. It is caused by the flagellated protozoan parasite Trichomonas vaginalis. […] The mechanism of metronidazole resistance in T. vaginalis from treatment failures is not well understood, unlike resistance which is developed in the laboratory under increasing metronidazole pressure. In the latter situation, hydrogenosomal function which is involved in activation of the prodrug, metronidazole, is down-regulated. […] Although anaerobic resistance has been regarded as a laboratory induced phenomenon, it clearly has been demonstrated in clinical isolates. […] Metronidazole enters both the cell and organelle via passive diffusion as a prodrug and competes with the terminal enzyme hydrogenase as an electron acceptor from Fd. Activation of the drug occurs when an electron is transferred to the all important nitro-group forming a toxic nitro-radical.

• #93 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Trichomoniasis is the most common, sexually transmitted infection. It is caused by the flagellated protozoan parasite Trichomonas vaginalis. […] The mechanism of metronidazole resistance in T. vaginalis from treatment failures is not well understood, unlike resistance which is developed in the laboratory under increasing metronidazole pressure. In the latter situation, hydrogenosomal function which is involved in activation of the prodrug, metronidazole, is down-regulated. […] Although anaerobic resistance has been regarded as a laboratory induced phenomenon, it clearly has been demonstrated in clinical isolates. […] Metronidazole enters both the cell and organelle via passive diffusion as a prodrug and competes with the terminal enzyme hydrogenase as an electron acceptor from Fd. Activation of the drug occurs when an electron is transferred to the all important nitro-group forming a toxic nitro-radical.

• #94 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Clinical isolates derived from treatment failures typically show resistance to metronidazole under aerobic conditions while some also exhibit anaerobic resistance. […] Anaerobic or complete resistance is selectively developed in vitro by continuously culturing trophozoites in increasing concentrations of metronidazole. […] Downregulation of hydrogenosomal function is not the only change observed in our highly metronidazole-resistant lines. […] The overexpression of Pgps is directly linked to the multiple drug resistance (MDR) phenotype observed in both mammalian tumour cells and the protozoan parasites Entamoeba and Leishmania. […] Cross-resistance among 5-nitroimidazole derivatives has been broadly observed in T. vaginalis isolates.

• #95 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Clinical isolates derived from treatment failures typically show resistance to metronidazole under aerobic conditions while some also exhibit anaerobic resistance. […] Anaerobic or complete resistance is selectively developed in vitro by continuously culturing trophozoites in increasing concentrations of metronidazole. […] Downregulation of hydrogenosomal function is not the only change observed in our highly metronidazole-resistant lines. […] The overexpression of Pgps is directly linked to the multiple drug resistance (MDR) phenotype observed in both mammalian tumour cells and the protozoan parasites Entamoeba and Leishmania. […] Cross-resistance among 5-nitroimidazole derivatives has been broadly observed in T. vaginalis isolates.

• #96 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Clinical isolates derived from treatment failures typically show resistance to metronidazole under aerobic conditions while some also exhibit anaerobic resistance. […] Anaerobic or complete resistance is selectively developed in vitro by continuously culturing trophozoites in increasing concentrations of metronidazole. […] Downregulation of hydrogenosomal function is not the only change observed in our highly metronidazole-resistant lines. […] The overexpression of Pgps is directly linked to the multiple drug resistance (MDR) phenotype observed in both mammalian tumour cells and the protozoan parasites Entamoeba and Leishmania. […] Cross-resistance among 5-nitroimidazole derivatives has been broadly observed in T. vaginalis isolates.

• #97 Transcriptional profile of Trichomonas vaginalis in response to metronidazole | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09339-9

  Trichomoniasis caused by Trichomonas vaginalis, combined with its complications, has long frequently damaged millions of human health. […] Therefore, a better understanding of its trichomonacidal process to ultimately reveal the global mechanism of action is indispensable. […] The RNA-seq data revealed a total of 10,937 differentially expressed genes (DEGs), consisting of 4,978 upregulated and 5,959 downregulated genes. […] Most DEGs for the known MTZ activators, such as pyruvate:ferredoxin oxidoreductase (PFOR) and iron-sulfur binding domain, were significantly downregulated. […] However, genes for other possible alternative MTZ activators such as thioredoxin reductase, nitroreductase family proteins and flavodoxin-like fold family proteins, were dramatically stimulated. […] GO and KEGG analyses revealed that genes for basic vital activities, proteostasis, replication and repair were stimulated under MTZ stress, but those for DNA synthesis, more complicated life activities such as the cell cycle, motility, signaling and even virulence were significantly inhibited in T. vaginalis.

• #98 Transcriptional profile of Trichomonas vaginalis in response to metronidazole | BMC Genomics | Full Text

  https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-023-09339-9

  A previous study concluded that a strong correlation existed between the presence of PFOR activity and MTZ among different microorganisms. […] Therefore, as the key proteins for MTZ activation, the wide downregulation of PFOR was likely to be a self-rescue response at the early stage. […] However, one of three genes mapped to thioredoxin reductase and five of six DEGs encoding nitroreductase family proteins were significantly upregulated by approximately 3.8-to to even 739.3-fold. […] Thioredoxin reductase (with nitroreductase activity) and nitroreductase have been reported to play roles in activating MTZ against T. vaginalis depending on an alternative theory. […] The significantly enriched upregulated genes were mainly involved in the basic life process, similar to the GO analysis.

• #99 Drug resistance in the sexually transmitted protozoan Trichomonas vaginalis | Cell Research

  https://www.nature.com/articles/7290169

  Clinical isolates derived from treatment failures typically show resistance to metronidazole under aerobic conditions while some also exhibit anaerobic resistance. […] Anaerobic or complete resistance is selectively developed in vitro by continuously culturing trophozoites in increasing concentrations of metronidazole. […] Downregulation of hydrogenosomal function is not the only change observed in our highly metronidazole-resistant lines. […] The overexpression of Pgps is directly linked to the multiple drug resistance (MDR) phenotype observed in both mammalian tumour cells and the protozoan parasites Entamoeba and Leishmania. […] Cross-resistance among 5-nitroimidazole derivatives has been broadly observed in T. vaginalis isolates.

• #100 Infinity war: Trichomonas vaginalis and interactions with host immune response

  https://microbialcell.com/researcharticles/2023a-bongiorni-galego-microbial-cell/

  The transient receptor potential-like channel of T. vaginalis (TvTRPV), cysteine peptidase, and -actinin are currently cited as candidate targets for vaccine development. In this context, the understanding of mechanisms involved in the host-T. vaginalis interaction that elicit the immune response may contribute to the development of new targets to combat trichomoniasis. […] The pathogen-neutrophil interaction goes beyond cytokine production. This in vitro direct contact decreases the myeloid cell leukemia 1 (Mcl-1) expression, an anti-apoptotic protein previously associated with PMNs survival, and increases caspase-3 expression, a protein related to spontaneous apoptosis in neutrophils that triggers the acceleration of the apoptosis process. […] Interestingly, while live trophozoites enhanced the rate of neutrophil apoptosis, trichomonads lysate reduced it.

• #101 eCommons at Roseman University – Annual Research Symposium: Pharmacognosy and Trichomoniasis: A Scoping Review Protocol

  https://ecommons.roseman.edu/researchsymposium/2024/clinical_case_reports/3/

  Trichomoniasis, also called trich, is the most common non-viral sexually transmitted infection (STI). Its etiological agent is the protozoan parasite Trichomonas vaginalis, against which first-line antiparasitics usually work. However, resistance is on the rise. […] But research in recent years has begun to unravel correlations of trichomonal infections with a myriad of comorbidities, including infertility, cancers, the pathogenesis of AIDS, and pelvic inflammatory disease (PID). […] Between the rise of drug resistance and the incidence of these comorbidities, new treatments are needed.

• #102

  https://www-.grantome.com/grant/NIH/R01-AI069058-04

  Trichomonas vaginalis is the etiologic agent of the most common non-viral sexually transmitted infection (STI) worldwide and is the most prevalent parasite found in the US population. […] Despite its global medical importance, the molecular mechanisms underlying the pathogenesis of T. vaginalis are virtually unknown. […] We have demonstrated a role for the glycocalyx that coats the surface of this parasite in host cell adherence and cytotoxicity and have identified the first putative host cell receptor for T. vaginalis. […] To this end, we propose to (1) elucidate the structure of wild-type and mutant T. vaginalis surface glycoconjugates and lipophosphoglycan (LPG) as a step towards identifying novel enzymes involved in its assembly, (2) delete the serine palmitoyl transferase 2 (SPT2) gene to create LPG null mutants and determine the effect on adherence and cytotoxicity of the parasite (3) validate candidate T. vaginalis genes required for the synthesis and assembly of the monosaccharide rhamnose, an unusual sugar that is absent in host cells and (4) examine the interaction between T. vaginalis LPG and host cell galectin-1 (gal-1) and investigate whether this interaction plays a role in pathogenesis. […] In addition to providing critical data on the mechanisms underlying host-pathogen interaction of this prevalent STI, the proposed studies will yield information that may be useful for developing novel drug therapies and vaccination strategies.

• #103 Infinity war: Trichomonas vaginalis and interactions with host immune response

  https://microbialcell.com/researcharticles/2023a-bongiorni-galego-microbial-cell/

  T. vaginalis has enzymes known as ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase) and ecto-5-nucleotidase (E-5N). They are responsible for a cascade that hydrolyzes extracellular nucleotides from tri-, di-, and monophosphate nucleotides to the nucleosides, such as ATP, ADP, and AMP to adenosine (ADO). […] In conclusion, NTPDases, E-5N, and adenosine deaminase provide the parasites with enzymatic mechanisms to modulate the inflammatory environment, contributing to parasite survival.

• #104 eCommons at Roseman University – Annual Research Symposium: Pharmacognosy and Trichomoniasis: A Scoping Review Protocol

  https://ecommons.roseman.edu/researchsymposium/2024/clinical_case_reports/3/

  Trichomoniasis, also called trich, is the most common non-viral sexually transmitted infection (STI). Its etiological agent is the protozoan parasite Trichomonas vaginalis, against which first-line antiparasitics usually work. However, resistance is on the rise. […] But research in recent years has begun to unravel correlations of trichomonal infections with a myriad of comorbidities, including infertility, cancers, the pathogenesis of AIDS, and pelvic inflammatory disease (PID). […] Between the rise of drug resistance and the incidence of these comorbidities, new treatments are needed.

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