Trichinoza
Patofizjologia i mechanizm

Trichinoza, wywoływana przez nicienie Trichinella spiralis, jest chorobą pasożytniczą o złożonym cyklu życiowym obejmującym fazę jelitową, migracyjną i mięśniową. Po spożyciu surowego lub niedogotowanego mięsa zawierającego otorbione larwy, larwy L1 uwalniane są w żołądku, dojrzewają w jelicie cienkim do dorosłych form, które po kopulacji produkują larwy noworodkowe (NBL). Larwy te migrują przez ścianę jelita do naczyń limfatycznych i krwionośnych, rozprzestrzeniając się do różnych narządów, jednak tylko te, które osiedlają się w mięśniach poprzecznie prążkowanych, tworzą charakterystyczne komórki pielęgnujące (nurse cells) otoczone kapsułą kolagenową, umożliwiającą przetrwanie larw przez wiele lat. Patogeneza obejmuje uszkodzenia mięśni, wątroby, serca i mózgu, a odpowiedź immunologiczna gospodarza przechodzi od fazy Th1 w jelicie do dominującej odpowiedzi Th2 w mięśniach, z udziałem cytokin IL-5, IL-10, IL-13 oraz eozynofilii. Ciężkość choroby zależy od dawki infekcyjnej, wieku, stanu immunologicznego i gatunku Trichinella.

Patogeneza Trichinellozy (Trichinoza)

Trichinoza to pasożytnicza choroba odzwierzęca wywołana przez nicienie z rodzaju Trichinella, głównie Trichinella spiralis. Szacuje się, że ponad 11 milionów ludzi na świecie jest zakażonych tymi pasożytami, a infekcja może występować w różnych stopniach nasilenia – od przypadków bezobjawowych po ciężkie manifestacje choroby, a nawet zgon.12

Charakterystyczną cechą epidemiologii T. spiralis jest obowiązkowe przenoszenie poprzez spożycie zakażonego mięsa. Głównym rezerwuarem pasożyta są świnie domowe, ale człowiek może zarazić się także poprzez spożycie niedogotowanego mięsa innych zwierząt, takich jak dziki, niedźwiedzie, dziki, konie, czy psy.34

Cykl życiowy Trichinella jako podstawa patogenezy

Trichinella ma unikalny, bezpośredni cykl życiowy, który nie wymaga pośrednich żywicieli stawonogowych. Zamiast tego, pasożyt rozprzestrzenia się poprzez spożycie zakażonego mięsa zawierającego otorbione larwy.5 Cykl życiowy można podzielić na trzy główne fazy: jelitową (enteral), migracyjną oraz mięśniową (parenteralną).6

Faza jelitowa

Infekcja rozpoczyna się, gdy człowiek spożywa surowe lub niedogotowane mięso zawierające otorbione larwy Trichinella. W żołądku, pod wpływem kwasu solnego i pepsyny, otoczki cyst (kapsuły) zostają rozpuszczone, co prowadzi do uwolnienia larw pierwszego stadium (L1).78

Uwolnione larwy przedostają się do jelita cienkiego, gdzie wnikają do nabłonka walcowatego i w ciągu około 30 godzin przechodzą cztery linienia, rozwijając się w dojrzałe samce i samice. Po około 5-7 dniach od infekcji dochodzi do kopulacji. Dorosłe samice są żyworodne – produkują nowe larwy (NBL – newborn larvae), które rozpoczynają inwazję.910

Faza jelitowa może przebiegać bezobjawowo lub powodować objawy ze strony przewodu pokarmowego, takie jak ból brzucha, biegunka, nudności i wymioty. Dorosłe samice produkują larwy przez około 4-6 tygodni, a następnie umierają lub są wydalane.1112

Faza migracyjna

Nowo narodzone larwy posiadają w jamie ustnej stylet, który wykorzystują do penetracji przez błonę śluzową jelita cienkiego. Larwy przechodzą przez ścianę jelita do naczyń limfatycznych i krwionośnych, a następnie są transportowane z krwią do różnych narządów i tkanek. Penetracja przez naczynia krwionośne odbywa się w sposób przypadkowy, co oznacza, że larwy mogą dotrzeć do niemal każdego organu.1314

Ta faza choroby związana jest z ogólnoustrojową reakcją zapalną, gorączką i eozynofilią. Larwy mogą znajdować się w różnych narządach, powodując zapalenie i martwicę, ale tylko te, które docierają do włókien mięśni poprzecznie prążkowanych, są w stanie przetrwać i rozwinąć się.1516

Faza mięśniowa

Larwy, które docierają do mięśni poprzecznie prążkowanych, wnikają do pojedynczych komórek mięśniowych, gdzie rosną i rozwijają się wykładniczo. Proces ten powoduje częściowe zniszczenie włókien mięśniowych i rozpoczyna złożony proces tworzenia komórki pielęgnującej (nurse cell).17

W ciągu 15-20 dni po infekcji larwy zwijają się spiralnie (co dało nazwę T. spiralis) i zostają otoczone kapsułą kolagenową tworzoną przez gospodarza. Ten proces otorbienia jest kompletny po około 4-5 tygodniach i umożliwia larwom przetrwanie w mięśniach przez wiele lat.1819

Larwy najczęściej lokalizują się w mięśniach o wysokiej aktywności metabolicznej, takich jak przepona, mięśnie języka, mięśnie żwaczy, mięśnie międzyżebrowe, mięśnie oka oraz mięśnie kończyn.2021

Transformacja komórki mięśniowej w komórkę pielęgnującą

Jednym z najbardziej fascynujących aspektów patogenezy trichinelozy jest tworzenie kompleksu komórki pielęgnującej (nurse cell). Jest to niezwykła adaptacja, w której pasożyt przekształca komórkę mięśniową gospodarza, aby stworzyć sprzyjające środowisko dla swojego przetrwania.22

Larwa przenika do komórki mięśniowej, przerywa błonę komórkową i zagnieżdża się w cytoplazmie. Następnie indukuje specyficzne zmiany morfologiczne w komórce gospodarza, takie jak:23

  • Wpływ na metabolizm komórki
  • Zmiana biosyntezy DNA
  • Zwiększenie produkcji kolagenu
  • Zwiększenie produkcji czynnika wzrostu naskórka (EGF)

24

Tworzenie komórki pielęgnującej odbywa się w środowisku hipoksycznym otaczającym nowo tworzone naczynia. Hipoksja stymuluje komórki mięśniowe w otaczającej tkance do zwiększenia ekspresji i wydzielania angiogennych cytokin, takich jak naczyniowo-śródbłonkowy czynnik wzrostu (VEGF). Pozwala to migrującej larwie T. spiralis na wniknięcie do miocytu i indukcję transformacji w komórkę pielęgnującą.25

W wyniku tych wszystkich zmian powstaje ochronna osłona kolagenowa, która chroni larwę przed komórkami układu immunologicznego gospodarza i zapewnia odżywianie pasożyta. Komórka mięśniowa poddana tym zmianom nazywana jest komórką pielęgnującą.26

Dzięki temu kompleksowi komórka pielęgnująca wydaje się być nienaruszona i aktywna przez lata, pomimo wewnątrzkomórkowego pasożytnictwa.27

Mechanizmy immunologiczne w patogenezie trichinelozy

Odpowiedź immunologiczna gospodarza na inwazję Trichinella jest złożona i obejmuje zarówno mechanizmy wrodzonej, jak i nabytej odporności.28

Odpowiedź immunologiczna w fazie jelitowej

Podczas fazy jelitowej obserwuje się początkowo odpowiedź typu Th1, charakteryzującą się znaczącym wzrostem cytokin Th1, takich jak IL-12, INF-γ, IL-1β i TNF-α. Produkcja tych cytokin jest bezpośrednio związana z rozwojem reakcji zapalnej i patologią jelitową, co paradoksalnie sprzyja infekcji przez T. spiralis.29

Badania wykazały, że egzogenne podanie IL-12 w infekcji T. spiralis hamuje jelitową mastocytozę, opóźnia wydalanie pasożyta i zwiększa obciążenie pasożytnicze mięśni. TNF-α jest silną cytokiną prozapalną, która odgrywa kluczową rolę w patogenezie chorób zapalnych, ponieważ uczestniczy w aktywacji kaskady cytokin prozapalnych.30

Mechanizm ekspulsji dorosłych nicieni T. spiralis z jelita jest inicjowany przez specyficzną reakcję nadwrażliwości typu opóźnionego. Wynikające z tego uszkodzenie tkanki dostarcza bodźców do zainicjowania niespecyficznego zapalenia alergicznego, co z kolei bezpośrednio wpływa na wydalenie robaków, prawdopodobnie z powodu stworzenia nieodpowiedniego środowiska biochemicznego.31

Istotnym mechanizmem usuwania pasożytów jelitowych jest tzw. „Weep and Sweep” (płacz i zamiatanie). Jest to zintegrowana odpowiedź obejmująca układy nerwowy, endokrynny i immunologiczny, która prowadzi do zwiększenia nawodnienia jelita i skurczów mięśni, powodując oddzielenie robaków od jelita i ich wydalenie poza organizm.32

Odpowiedź immunologiczna w fazie mięśniowej

Immunologiczna odpowiedź na inwazję mięśniową T. spiralis charakteryzuje się głównie fenotypem Th2. Komórki pobrane z szyjnych węzłów chłonnych zakażonych myszy produkują IL-5, IL-10, IL-13 i IFN-γ po stymulacji somatycznymi antygenami larwalnymi.33

U myszy z wyłączonym genem interleukiny-10 (IL-10) (IL10-/-) zakres nacieku zapalnego wokół komórki pielęgnującej był znacznie większy w porównaniu z myszami kontrolnymi podczas ostrej fazy infekcji, chociaż skład komórkowy pozostawał ten sam.34

Rola eozynofilów w doświadczalnej trichinellozie wskazuje, że larwy mięśniowe są uszkadzane przez odpowiedź immunologiczną kierowaną przez komórki Th1, które wydają się być hamowane przez eozynofile. Dla pasożyta korzystne jest wywołanie u gospodarza odpowiedzi Th2 prowadzącej do eozynofilii tkankowej podczas fazy mięśniowej infekcji.35

Synteza i uwalnianie IL-4 i IL-13 indukują proliferację komórek B i ekspresję antygenów powierzchniowych, w tym receptora CD23 (FcRII) o niskim powinowactwie do IgE i cząsteczek MHC klasy II, stymulując produkcję IgE.36

Mechanizmy uszkodzenia narządów wewnętrznych

Chociaż larwy Trichinella preferują osiedlanie się w mięśniach szkieletowych, mogą również powodować uszkodzenia innych narządów podczas fazy migracyjnej. Mechanizmy leżące u podstaw uszkodzenia narządów wewnętrznych są nadal przedmiotem debaty.37

Teoria czysto mechaniczna sugeruje, że larwy powodują okluzję małych tętniczek mózgowych, co prowadzi do dystalnego niedokrwienia. Jednak chociaż bezpośrednia inwazja mięśnia sercowego i miąższu mózgu przez T. spiralis była oczywista, otorbienie larw w tych narządach było zgłaszane tylko w rzadkich przypadkach.38

Uszkodzenie narządów wewnętrznych może wynikać z:39

  • Bezpośredniego uszkodzenia – przez migrujące larwy
  • Pośredniego uszkodzenia – poprzez mechanizmy immunologiczne lub eozynofilię
  • Przewlekłego przebiegu choroby – który może prowadzić do nieodwracalnych uszkodzeń

40

Patogeneza zajęcia wątroby jest spowodowana penetracją larw do zatok wątrobowych. Zmiany w wątrobie mogą być widoczne w trakcie lub po fazie jelitowej. Enzymy wątrobowe są uwalniane do krwi obwodowej w większych ilościach niż ich normalne stężenia, gdy dochodzi do uszkodzenia błony komórkowej hepatocytów, co skutkuje zwiększoną przepuszczalnością.41

Uszkodzenie mięśnia sercowego

Zajęcie mięśnia sercowego przez Trichinella może prowadzić do zapalenia mięśnia sercowego (myocarditis) i niewydolności serca, co jest jednym z najpoważniejszych powikłań trichinelozy.42

Larwy w mięśniu sercowym i innych narządach, takich jak mózg, powodują obrzęk, martwicę i ogniskowe nacieki neutrofilów, eozynofilów i limfocytów, ale nie otorbiają się.43

Zajęcie ośrodkowego układu nerwowego

Uszkodzenie mózgu przez migrujące larwy może prowadzić do zapalenia opon mózgowo-rdzeniowych i mózgu, co jest również potencjalnie śmiertelnym powikłaniem trichinelozy.44

W ciężkich przypadkach trichinelozy (masywna inwazja) śmierć może nastąpić w wyniku zapalenia mięśnia sercowego, niewydolności serca, zapalenia opon mózgowo-rdzeniowych lub zapalenia mózgu.45

Czynniki wpływające na nasilenie choroby

Nasilenie objawów klinicznych trichinelozy jest silnie zależne i bezpośrednio skorelowane z kilkoma czynnikami:46

  • Liczbą spożytych larw T. spiralis
  • Wiekiem i płcią osoby zakażonej
  • Rodzajem zajętej tkanki
  • Stanem odżywienia
  • Statusem hormonalnym
  • Statusem immunologicznym

4748

Dotkliwość choroby jest związana z dawką infekcyjną i charakterystyką gospodarza, taką jak wiek pacjenta lub przygotowanie immunologiczne w wyniku wcześniejszej infekcji Trichinella. Niektóre doniesienia łączą ciężkość choroby z infekującym gatunkiem Trichinella, sugerując, że niektóre gatunki są bardziej skłonne do wywoływania ciężkiej choroby niż inne.49

Implikacje patogenezy dla diagnostyki i leczenia

Zrozumienie patogenezy trichinelozy ma kluczowe znaczenie dla skutecznej diagnostyki i leczenia tej choroby. Diagnostyka trichinelozy może obejmować:5051

  • Badania serologiczne wykrywające przeciwciała przeciwko Trichinella
  • Biopsję mięśni w celu identyfikacji otorbionych lub nieotorbionych larw
  • Badania mikroskopowe

5253

Biopsje mięśni są rzadko wykonywane, ale pozwalają na molekularną identyfikację gatunku lub genotypu Trichinella, co nie jest możliwe za pomocą testów na przeciwciała. Zwykle pobiera się 0,2 do 0,5 grama ludzkiej lub zwierzęcej tkanki mięśniowej szkieletowej i bada na obecność larw Trichinella za pomocą sztucznego trawienia lub analizy histologicznej.54

Leczenie trichinelozy opiera się na stosowaniu leków przeciwpasożytniczych, takich jak albendazol lub mebendazol, które są skuteczne w eliminacji dorosłych robaków z przewodu pokarmowego, jeśli leczenie rozpocznie się odpowiednio wcześnie. Jednak skuteczność tych leków wobec otorbionych larw w mięśniach jest ograniczona.5556

Jeśli leczenie rozpocznie się w ciągu pierwszych 3 dni infekcji, można zapobiec inwazji mięśniowej i progresji choroby. Nie ma jednak skutecznego leczenia, gdy larwy są już otorbione w mięśniach.5758

W przypadkach ciężkiej trichinelozy, gdy występuje masowa inwazja, obok leków przeciwpasożytniczych stosuje się często leki przeciwzapalne i kortykosteroidy, aby kontrolować ból i obrzęk spowodowane reakcją zapalną organizmu.59

Strategie unikania odpowiedzi immunologicznej przez Trichinella

Infekcja Trichinella spiralis może powodować odzwierzęcą trichineloze, która poważnie zagraża zdrowiu ludzi. Mechanizm unikania odpowiedzi immunologicznej, jako powszechny mechanizm doboru naturalnego, jest adaptacją patogenów do układu odpornościowego. Umożliwia patogenom złagodzenie odpowiedzi immunologicznej gospodarza, uniknięcie ataku ze strony układu odpornościowego i zapewnienie przetrwania i rozmnażania.60

Dalsze badania nad mechanizmem unikania odpowiedzi immunologicznej Trichinella spiralis mają duże znaczenie dla zapobiegania i kontroli trichinelozy, leczenia ludzkich chorób autoimmunologicznych i chorób alergicznych.61

Podsumowanie kluczowych mechanizmów patogenezy

Patogeneza trichinelozy jest złożonym procesem, który obejmuje:6263

  • Fazę jelitową – uwolnienie larw w żołądku, migracja do jelita cienkiego, dojrzewanie do postaci dorosłych, produkcja nowych larw
  • Fazę migracyjną – przenikanie larw przez ścianę jelita do układu limfatycznego i krwionośnego
  • Fazę mięśniową – osiedlanie się larw w mięśniach szkieletowych, tworzenie komórek pielęgnujących
  • Złożoną odpowiedź immunologiczną – początkowo typu Th1, a następnie dominację typu Th2
  • Strategię unikania odpowiedzi immunologicznej przez pasożyta poprzez modulację odpowiedzi gospodarza
  • Uszkodzenie narządów wewnętrznych – zarówno przez bezpośrednią inwazję larw, jak i pośrednio przez mechanizmy immunologiczne

6465

Niedawne badania zidentyfikowały nową proteazę serynową Trichinella spiralis (TsSPc), która odgrywa rolę w inwazji jelitowej. TsSPc wiąże się z receptorem RACK1 w nabłonku jelitowym, aktywuje szlak MAPK/ERK1/2, zmniejsza ekspresję białek ścisłych połączeń (TJs) jelitowych i niszczy integralność nabłonka, przez co pośredniczy w inwazji larw T. spiralis w błonie śluzowej jelita.66

Zrozumienie złożonych mechanizmów patogenezy trichinelozy jest kluczowe dla opracowania skuteczniejszych strategii diagnostycznych, terapeutycznych i profilaktycznych w walce z tą chorobą pasożytniczą.67

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  1. 09.04.2026
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Materiały źródłowe

  • #1 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    Currently, it is estimated that more than 11 million humans in the world are infected by helminth parasites of Trichinella species, mainly by Trichinella spiralis (T. spiralis), responsible for causing Trichinellosis disease in both animals and humans. […] Trichinellosis is a cosmopolitan parasitic zoonotic disease, which has direct relevance to human and animal health, because it presents a constant and important challenge to the hosts immune system, especially through the intestinal tract. […] The main characteristic of the epidemiology of T. spiralis is its obligatory transmission by ingestion of infected meat. […] When a host ingests meat infected with L1 of T. spiralis (T. spiralis-L1), the digestive juices of the stomach dissolve the collagen capsule, also called nurse cell (NC), releasing the T. spiralis-L1, which travel to the small intestine, where they invade the columnar epithelium, giving rise to the intestinal phase of the infection.
  • #2 Trichinellosis – WOAH – World Organisation for Animal Health
    https://www.woah.org/en/disease/trichinellosis/
    Trichinellosis is a serious zoonotic disease (an animal disease that can infect humans) caused by parasitic nematodes (roundworms) of the genus Trichinella. […] An infected human or animal has larvae lodged in its muscle. When a person or animal eats meat which is infected, the larvae are released from the muscle as it is digested and rapidly develop into adults in the intestine of the new host. The adult worms reproduce and produce live larvae that penetrate the wall of the intestine and travel via the lymphatic and blood system throughout the body to finally enter muscle cells. In some Trichinella species the cells turned nurse cells form cysts that can remain viable for years. […] Trichinella is very prolific and an infected animal might have up to several hundred larvae per gram of muscle. The life cycle in animals can continue as larvae are able to survive in decaying carcasses for a long time, facilitating transmission by scavenging. […] On the other hand, humans are a dead end for the parasite.
  • #3 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    Currently, it is estimated that more than 11 million humans in the world are infected by helminth parasites of Trichinella species, mainly by Trichinella spiralis (T. spiralis), responsible for causing Trichinellosis disease in both animals and humans. […] Trichinellosis is a cosmopolitan parasitic zoonotic disease, which has direct relevance to human and animal health, because it presents a constant and important challenge to the hosts immune system, especially through the intestinal tract. […] The main characteristic of the epidemiology of T. spiralis is its obligatory transmission by ingestion of infected meat. […] When a host ingests meat infected with L1 of T. spiralis (T. spiralis-L1), the digestive juices of the stomach dissolve the collagen capsule, also called nurse cell (NC), releasing the T. spiralis-L1, which travel to the small intestine, where they invade the columnar epithelium, giving rise to the intestinal phase of the infection.
  • #4 Trichinosis – Knowledge and References – Taylor & Francis
    https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Infectious_diseases/Trichinosis/
    Trichinosis is a parasitic infection caused by nematodes of the genus Trichinella, which is acquired by consuming undercooked meat, particularly pork or bear. The clinical manifestations of trichinosis include months of nausea, vomiting, and diarrhea without blood or mucus, followed by high fever, periorbital edema, myalgias, muscle masses, and CN palsies. […] Trichinosis has a worldwide distribution, but is most prevalent in Europe and North America. The adult Trichinella spiralis are 1 to 4mm in length. The female is viviparous, delivering larvae; thus, there is no external egg stage. All carnivorous species, including humans, are the definitive hosts. Most human infections result from ingestion of inadequately cooked meat. Bear, wild pig, boar, horse, and dog meat are the usual sources, but pork is the most common cause in the United States. Adult worms, living in the small intestine, release larvae into the mucosal epithelium. The larvae enter the bloodstream and migrate to muscle tissue, where they embed and mature to the infective stage. A cyst envelops the larva, and it remains infective until the cyst calcifies, killing the larva. When meat containing encysted larvae is ingested, the cysts are dissolved by gastric secretions, and the infective larvae are released. Within 36 hours, maturation occurs, and within a week larvae are produced, to become encysted in this new host. Diagnosis of trichinosis is based on the history of ingestion of undercooked meat and a compatible clinical picture. Definitive diagnosis requires either laboratory detection of specific antibodies or muscle biopsy finding encysted larvae.
  • #5 Trichinosis (Trichinellosis): Background, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/230490-overview
    Trichinella species require two hosts to sustain their life cycles, spreading through the ingestion of infected flesh rather than relying on traditional arthropod intermediate hosts. […] The life cycle of Trichinella is maintained by animals that consume other animals containing encysted infective larvae in their striated muscles, such as pigs, horses, and predators such as bears, foxes, and boars. […] After ingestion, the larvae excyst in the small intestine, penetrate the mucosal lining, and develop into adults within 6 to 8 days, with females measuring about 2.2 mm and males around 1.2 mm. […] Mature females release live larvae for 4 to 6 weeks before dying or being expelled. […] The newborn larvae migrate through the bloodstream and lymphatic system, ultimately residing in striated skeletal muscle cells.
  • #6 Trichinosis | MedLink Neurology
    https://www.medlink.com/articles/trichinosis
    Trichinosis is caused by zoonotic infestation of nematode in the genus Trichinella. […] The life cycle of Trichinella includes: (1) enteric phase (the larvae enter the duodenal walls), (2) migratory phase (the newborn larvae penetrate through the intestinal walls into the lymphatic and blood vessels), and (3) parenteral phase (the larvae resume their lives as an intracellular parasite). […] During the migratory phase, the newborn larvae pass through the intestinal wall into the lymphatic vessels and circulatory system. Once in a capillary bed of a given tissue, the larvae penetrate the circulation in a random fashion. By this route, larvae can reach any organs, and then they seed and provoke an inflammatory reaction. […] During the parenteral phase, the larvae resume their lives as an intracellular parasite only in skeletal muscle. The infected striated muscle is transformed to nurse cells. This process takes 20 days to complete.
  • #7 Trichinella spiralis Infection – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK538511/
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] Enteric or gastrointestinal phase: After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Systemic (parenteral) phase: Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #8 Trichinella spiralis Infection | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/616
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #9 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    After 10-30 hours post-infection (pi), T. spiralis-L1 mature to female and male adult worms (AD). […] Approximately 7 days pi, copulation occurs between female and male AD. […] The NBL of T. spiralis possess a stylet in their oral cavity, which they use to internalize within the epithelial cells of the host, penetrating the submucosa of the small intestine, migrating mainly through the circulatory system to various organs and subsequently invading the musculoskeletal cells, causing tissue damage. […] Only the NBL of T. spiralis that invade the musculoskeletal cells can survive and grow, giving rise to the muscle phase of the infection. […] During the muscular phase, the NBL of T. spiralis are in the muscle fibers, destroying them partially, and begin a period of post-embryonic development, growing and developing exponentially.
  • #10 CDC – DPDx – Trichinellosis
    https://www.cdc.gov/dpdx/trichinellosis/index.html
    Trichinellosis (trichinosis) is caused by nematodes (roundworms) of the genus Trichinella. […] Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T. pseudospiralis and T. papuae, which do not encyst) of Trichinella species. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms. […] Diagnosis is usually made based on clinical symptoms, and is confirmed by serology or identification of encysted or non-encysted larvae in biopsy or autopsy specimens. […] The suspicion of trichinellosis (trichinosis), based on history, clinical symptoms, and eosinophilia, can be confirmed by specific diagnostic tests, including antibody detection, muscle biopsy, and microscopy.
  • #11 Trichinosis – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/nematodes-roundworms/trichinosis
    The Trichinella life cycle is maintained by animals that are fed (eg, pigs) or eat (eg, bears, foxes, boars) other animals whose striated muscles contain encysted infective larvae (eg, rodents). Humans become infected by eating undercooked meat from infected animals, most commonly pigs, wild boar, or bear. […] Larvae excyst in the small intestine, penetrate the mucosa, and become adults in 6 to 8 days. […] Mature females release living larvae for 4 to 6 weeks and then die or are expelled. Newborn larvae migrate through the bloodstream and lymphatics but ultimately survive only within striated skeletal muscle cells. Larvae fully encyst in 1 to 2 months and remain viable for several years as intracellular parasites. […] Anthelmintics eliminate adult Trichinella worms from the gastrointestinal tract, but once larvae encyst in skeletal muscle, treatment may not eradicate them or any associated symptoms. However, most people with trichinosis recover fully. […] The efficacy of higher doses and prolonged courses in killing encysted larvae is uncertain and adverse effects are more likely.
  • #12 Trichinosis (Trichinellosis): Background, Pathophysiology, Epidemiology
    https://emedicine.medscape.com/article/230490-overview
    Trichinella species require two hosts to sustain their life cycles, spreading through the ingestion of infected flesh rather than relying on traditional arthropod intermediate hosts. […] The life cycle of Trichinella is maintained by animals that consume other animals containing encysted infective larvae in their striated muscles, such as pigs, horses, and predators such as bears, foxes, and boars. […] After ingestion, the larvae excyst in the small intestine, penetrate the mucosal lining, and develop into adults within 6 to 8 days, with females measuring about 2.2 mm and males around 1.2 mm. […] Mature females release live larvae for 4 to 6 weeks before dying or being expelled. […] The newborn larvae migrate through the bloodstream and lymphatic system, ultimately residing in striated skeletal muscle cells.
  • #13 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    After 10-30 hours post-infection (pi), T. spiralis-L1 mature to female and male adult worms (AD). […] Approximately 7 days pi, copulation occurs between female and male AD. […] The NBL of T. spiralis possess a stylet in their oral cavity, which they use to internalize within the epithelial cells of the host, penetrating the submucosa of the small intestine, migrating mainly through the circulatory system to various organs and subsequently invading the musculoskeletal cells, causing tissue damage. […] Only the NBL of T. spiralis that invade the musculoskeletal cells can survive and grow, giving rise to the muscle phase of the infection. […] During the muscular phase, the NBL of T. spiralis are in the muscle fibers, destroying them partially, and begin a period of post-embryonic development, growing and developing exponentially.
  • #14 Trichinosis – UF Health
    https://ufhealth.org/conditions-and-treatments/trichinosis
    Trichinosis is a parasitic disease caused by eating meat that has not been thoroughly cooked and contains cysts (larvae, or immature worms) of Trichinella spiralis. […] When a person eats meat from an infected animal, trichinella cysts break open in the intestine and grow into adult roundworms. The roundworms produce other worms that move through the gut wall and into the bloodstream. The worms invade muscle tissues, including the heart and diaphragm (the breathing muscle under the lungs). They can also infect the lungs and brain. The cysts can remain alive for years. […] The cysts hatch in the intestines and produce large numbers of larvae that migrate into muscle tissue. The cysts may cause muscle pain and swelling in the face and around the eyes.
  • #15 Trichinellosis – Helminthiases – Parasitic Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.69.3.
    Trichinellosis (trichinosis) is a systemic inflammatory parasitic zoonosis that involves the skeletal muscles and causes allergic vasculitis. […] Larvae present in contaminated meat consumed by the patient enter the intestinal mucosa, within ~48 hours transform into the adult form, and after subsequent 5 to 6 days start producing new larvae (for ~5 weeks). The larvae enter the intestinal blood vessels and lymphatic vessels and are carried by bloodstream to various organs (mainly skeletal muscles with a high metabolic rate: tongue, diaphragm, as well as intercostal muscles, masseter muscle, extraocular muscles, neck muscles, and flexor muscles of the extremities). In the muscles the larvae encyst in a capsule produced by the host (termed a nurse cell), where they may survive up to a few years. In cell types other than the skeletal muscle the larvae are not able to encyst and continue to migrate, thus causing inflammation and necrosis.
  • #16 Trichinosis – Wikipedia
    https://en.wikipedia.org/wiki/Trichinosis
    The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. […] The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host.
  • #17 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    After 10-30 hours post-infection (pi), T. spiralis-L1 mature to female and male adult worms (AD). […] Approximately 7 days pi, copulation occurs between female and male AD. […] The NBL of T. spiralis possess a stylet in their oral cavity, which they use to internalize within the epithelial cells of the host, penetrating the submucosa of the small intestine, migrating mainly through the circulatory system to various organs and subsequently invading the musculoskeletal cells, causing tissue damage. […] Only the NBL of T. spiralis that invade the musculoskeletal cells can survive and grow, giving rise to the muscle phase of the infection. […] During the muscular phase, the NBL of T. spiralis are in the muscle fibers, destroying them partially, and begin a period of post-embryonic development, growing and developing exponentially.
  • #18 Trichinosis pathophysiology – wikidoc
    https://www.wikidoc.org/index.php/Trichinosis_pathophysiology
    Trichinosis is acquired by ingesting meat containing cysts (encysted larvae) (life cycle stage: 1) of Trichinella. […] After exposure to gastric acid and pepsin, the larvae are released (life cycle stage: 2) from the cysts and invade the small bowel mucosa. […] The newborn larvae enter the lymphatic vessels and then enter the bloodstream. […] The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. […] Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable for several years (life cycle stage: 5).
  • #19 Trichinellosis in Animals – Generalized Conditions – Merck Veterinary Manual
    https://www.merckvetmanual.com/generalized-conditions/trichinellosis/trichinellosis-in-animals
    Infection occurs by means of ingestion of larvae that parasitize striated muscle cells. The cyst wall is digested in the stomach, and the free larvae penetrate the duodenal and jejunal mucosa. Within ~4 days, the larvae develop into sexually mature adults. After mating, the females (34 mm) penetrate deeper into the mucosa and discharge living larvae (up to 1,500) throughout 416 weeks. After reproduction, the adult worms die and usually are digested. The young larvae (0.1 mm) migrate into the lymphatics, are carried via the portal system into the peripheral circulation, and reach striated muscle, where they penetrate individual muscle cells. They grow rapidly (to 1 mm) and begin to coil within the cell, usually one per cell. […] In encapsulated taxa, capsule formation begins ~15 days after infection and is completed by 48 weeks, at which time the larvae are infective. Infected cells degenerate as the larva grows, followed by calcification which occurs at different rates in various hosts. Larvae may remain viable within cysts for years and their development continues only if ingested by another suitable host. The diaphragm, tongue, masseter, and intercostal muscles are among those most frequently infected in pigs.
  • #20 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The NC formation process is a complex process and includes the cellular response of the infected muscle and the responses of the NC. […] This explains why CN seems intact and active for years despite intracellular parasitism. […] The main striated muscles where the L1-T. spiralis is implanted are the most active such as the diaphragm, masseters, intercostals, eye muscles, muscles of the tongue, and anterior and posterior extremities. […] The severity of the clinical disease is strongly dependent and directly correlated with the number of L1-T. spiralis ingested, age, sex, invaded tissue, nutritional, hormonal and immune status. […] The clinical pathology of Trichinellosis can be divided based on the phases of the T. spiralis life cycle. […] The Th1 type immune response against T. spiralis is characterized by a significant increase in Th1 cytokines such as IL-12, INF-, IL-1 and TNF-.
  • #21 Trichinella/Trichinellosis | Concise Medical Knowledge
    https://www.lecturio.com/concepts/trichinella-trichinellosis/
    Encysted larvae live within the striated muscles of the reservoir animal (some species are not encysted). […] Larvae are ingested when undercooked meat is consumed. […] After exposure to gastric acid and pepsin, larvae are released from the cysts. […] Larvae invade small-bowel mucosa and then become adult worms. […] Mating occurs; life span in the small bowel lasts approximately 4 weeks. […] Females release larvae that enter circulation. […] Larvae migrate to striated muscles. […] Tissue migration can last up to 1 month, causing symptoms. […] Highly active muscles affected include diaphragm, tongue, masseter, intercostals, and extraocular muscles. […] Can reach myocardium and the brain and lead to cardiac and cerebral inflammatory reaction. […] As larvae encyst, tissue infiltration (by PMNs and eosinophils) and edema occur. […] Calcification follows after a period of months, and after that, they remain in that state for years, but symptoms decrease after months.
  • #22 Trichinella spiralis – Wikipedia
    https://en.wikipedia.org/wiki/Trichinella_spiralis
    The migration and encystment of larvae can cause fever and pain, brought on by the host inflammatory response. In some cases, accidental migration to specific organ tissues can cause myocarditis and encephalitis that can result in death. […] Nurse cell formation in skeletal muscle tissue is mediated by the hypoxic environment surrounding the new vessel formation. The hypoxic environment stimulates muscle cells in the surrounding tissue to upregulate and secrete angiogenic cytokines, such as vascular endothelial growth factor (VEGF). This allows the migrating T. spiralis larva to enter the myocyte and induce the transformation into the nurse cell. VEGF expression is detected surrounding the nurse cell immediately after nurse cell formation, and the continued secretion of VEGF can maintain the constant state of hypoxia.
  • #23 Trichinellosis – WikiLectures
    https://www.wikilectures.eu/w/Trichinellosis
    The larva disrupts the cell membrane and nests in the cytoplasm. Here, it twists and causes specific morphological changes in the host cell as needed by the parasite – it affects metabolism, DNA biosynthesis, increases collagen and EGF production. The result is the formation of a collagen casing. […] All these changes lead to the protection of the larva from the body’s immune cells and also ensure the nutrition of the parasite larva. The cell thus changed is then called a nurse cell.
  • #24 Trichinellosis – WikiLectures
    https://www.wikilectures.eu/w/Trichinellosis
    The larva disrupts the cell membrane and nests in the cytoplasm. Here, it twists and causes specific morphological changes in the host cell as needed by the parasite – it affects metabolism, DNA biosynthesis, increases collagen and EGF production. The result is the formation of a collagen casing. […] All these changes lead to the protection of the larva from the body’s immune cells and also ensure the nutrition of the parasite larva. The cell thus changed is then called a nurse cell.
  • #25 Trichinella spiralis – Wikipedia
    https://en.wikipedia.org/wiki/Trichinella_spiralis
    The migration and encystment of larvae can cause fever and pain, brought on by the host inflammatory response. In some cases, accidental migration to specific organ tissues can cause myocarditis and encephalitis that can result in death. […] Nurse cell formation in skeletal muscle tissue is mediated by the hypoxic environment surrounding the new vessel formation. The hypoxic environment stimulates muscle cells in the surrounding tissue to upregulate and secrete angiogenic cytokines, such as vascular endothelial growth factor (VEGF). This allows the migrating T. spiralis larva to enter the myocyte and induce the transformation into the nurse cell. VEGF expression is detected surrounding the nurse cell immediately after nurse cell formation, and the continued secretion of VEGF can maintain the constant state of hypoxia.
  • #26 Trichinellosis – WikiLectures
    https://www.wikilectures.eu/w/Trichinellosis
    The larva disrupts the cell membrane and nests in the cytoplasm. Here, it twists and causes specific morphological changes in the host cell as needed by the parasite – it affects metabolism, DNA biosynthesis, increases collagen and EGF production. The result is the formation of a collagen casing. […] All these changes lead to the protection of the larva from the body’s immune cells and also ensure the nutrition of the parasite larva. The cell thus changed is then called a nurse cell.
  • #27 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The NC formation process is a complex process and includes the cellular response of the infected muscle and the responses of the NC. […] This explains why CN seems intact and active for years despite intracellular parasitism. […] The main striated muscles where the L1-T. spiralis is implanted are the most active such as the diaphragm, masseters, intercostals, eye muscles, muscles of the tongue, and anterior and posterior extremities. […] The severity of the clinical disease is strongly dependent and directly correlated with the number of L1-T. spiralis ingested, age, sex, invaded tissue, nutritional, hormonal and immune status. […] The clinical pathology of Trichinellosis can be divided based on the phases of the T. spiralis life cycle. […] The Th1 type immune response against T. spiralis is characterized by a significant increase in Th1 cytokines such as IL-12, INF-, IL-1 and TNF-.
  • #28 Trichinella inflammatory myopathy: host or parasite strategy? | Parasites & Vectors | Full Text
    https://parasitesandvectors.biomedcentral.com/articles/10.1186/1756-3305-4-42
    The immunological response to T. spiralis muscle invasion is mainly characterized by a Th2 phenotype, in fact cells collected from cervical lymph nodes of infected mice produce IL-5, IL-10, IL-13 and IFN- after stimulation with somatic larval antigens. […] In knock-out (KO) mice for the interleukin-10 (IL-10) gene (IL10-/-), the extent of the inflammatory infiltrate around the NC was markedly increased compared with control mice during the acute phase of infection, though the cellular composition remained the same. […] The role of eosinophils in experimental trichinellosis shows that muscle larvae are damaged by an immune response driven by Th1 cells which seem to be downregulated by eosinophils. […] Information derived from the studies on Trichinella-induced muscle inflammation provide new perspectives of the host-parasite relationship. For this reason it appears beneficial for the parasite to elicit in its host a Th2 response leading to tissue eosinophilia, during the muscle stage of infection.
  • #29 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    Studies have shown that the production of Th1 cytokines is directly associated with the development of the inflammatory response and intestinal pathology, which favors the infection by T. spiralis. […] However, exogenous administration of IL-12 in T. spiralis infection suppresses intestinal mastocytosis, delaying the expulsion of the parasite and increasing the parasitic muscle burden. […] TNF- is a potent proinflammatory cytokine, which plays a key role in the pathogenesis of inflammatory diseases, since it participates in the activation of a cascade of proinflammatory cytokines. […] Studies have shown that TSL-1 antigens are capable to induce the expression of iNOS with the consequent production of NO. […] However, NO production is also associated with the development of intestinal pathology in T. spiralis infection.
  • #30 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    Studies have shown that the production of Th1 cytokines is directly associated with the development of the inflammatory response and intestinal pathology, which favors the infection by T. spiralis. […] However, exogenous administration of IL-12 in T. spiralis infection suppresses intestinal mastocytosis, delaying the expulsion of the parasite and increasing the parasitic muscle burden. […] TNF- is a potent proinflammatory cytokine, which plays a key role in the pathogenesis of inflammatory diseases, since it participates in the activation of a cascade of proinflammatory cytokines. […] Studies have shown that TSL-1 antigens are capable to induce the expression of iNOS with the consequent production of NO. […] However, NO production is also associated with the development of intestinal pathology in T. spiralis infection.
  • #31 The Present Understanding of the Mechanism of Immunity to Trichinella Spiralis in: The American Journal of Tropical Medicine and Hygiene Volume 16 Issue 2 (1967)
    https://www.ajtmh.org/abstract/journals/tpmd/16/2/article-p123.xml
    Our present knowledge warrants the conclusion that the mechanism causing expulsion of adult T. spiralis is triggered by a specific delayed hypersensitivity reaction. […] The resultant tissue damage provides the stimuli for initiation of nonspecific allergic inflammation, which in turn directly effects expulsion of worms, probably due to the creation of an unsuitable biochemical environment. […] Further, the evidence indicates that humoral antibodies at best play only a minor role in the elimination of worms. Nevertheless, they are important in the total immunity in that they produce direct deleterious effects against the worms, such as interference with growth and reduction of the reproductive potential, and they are responsible for contributing to cellular destruction as a consequence of anaphylactic hypersensitivity reactions. […] Considerable work remains to clarify various aspects of the delayed response to T. spiralis, such as demonstration of the responsible antigen(s) and, by electron microscopy, the true identity of the immunologically competent cells.
  • #32 Pumpkin seeds (Cucurbita pepo subsp. ovifera) decoction promotes Trichinella spiralis expulsion during intestinal phase via “Weep and Sweep” mechanism | Scientific Reports
    https://www.nature.com/articles/s41598-024-51616-4
    Trichinosis is a zoonotic disease of communal health concern as it instigated human outbreaks in several countries. […] The pumpkin decoction’s anthelmintic action was facilitated by the TGF-1 and IL-17-driven Weep and Sweep mechanism. […] It has been demonstrated that having worms in the bowel causes a number of pathological alterations that cause acute inflammatory reactions in the small intestine. […] The goblet cell hyperplasia seen in Trichinella infections is a mucosal epithelial response to Th2 cytokines, primarily regulated by IL-13. […] To remove gastro-intestinal helminths an integrated response including the nervous, endocrine, and immune systems are used to expel the parasites. This is achieved by rising intestinal hydration and muscle contraction, which causes the worms to separate from the intestine and be released outside the body as part of a „Weep and Sweep” reaction. […] The Weep and Sweep mechanism is essential for the expulsion of Trichinella spiralis from the intestine. […] Pumpkin seeds decoction exhibited anthelmintic activity by two mechanisms: inducing weep and sweep processes and stimulating immunity Type 2.
  • #33 Trichinella inflammatory myopathy: host or parasite strategy? | Parasites & Vectors | Full Text
    https://parasitesandvectors.biomedcentral.com/articles/10.1186/1756-3305-4-42
    The immunological response to T. spiralis muscle invasion is mainly characterized by a Th2 phenotype, in fact cells collected from cervical lymph nodes of infected mice produce IL-5, IL-10, IL-13 and IFN- after stimulation with somatic larval antigens. […] In knock-out (KO) mice for the interleukin-10 (IL-10) gene (IL10-/-), the extent of the inflammatory infiltrate around the NC was markedly increased compared with control mice during the acute phase of infection, though the cellular composition remained the same. […] The role of eosinophils in experimental trichinellosis shows that muscle larvae are damaged by an immune response driven by Th1 cells which seem to be downregulated by eosinophils. […] Information derived from the studies on Trichinella-induced muscle inflammation provide new perspectives of the host-parasite relationship. For this reason it appears beneficial for the parasite to elicit in its host a Th2 response leading to tissue eosinophilia, during the muscle stage of infection.
  • #34 Trichinella inflammatory myopathy: host or parasite strategy? | Parasites & Vectors | Full Text
    https://parasitesandvectors.biomedcentral.com/articles/10.1186/1756-3305-4-42
    The immunological response to T. spiralis muscle invasion is mainly characterized by a Th2 phenotype, in fact cells collected from cervical lymph nodes of infected mice produce IL-5, IL-10, IL-13 and IFN- after stimulation with somatic larval antigens. […] In knock-out (KO) mice for the interleukin-10 (IL-10) gene (IL10-/-), the extent of the inflammatory infiltrate around the NC was markedly increased compared with control mice during the acute phase of infection, though the cellular composition remained the same. […] The role of eosinophils in experimental trichinellosis shows that muscle larvae are damaged by an immune response driven by Th1 cells which seem to be downregulated by eosinophils. […] Information derived from the studies on Trichinella-induced muscle inflammation provide new perspectives of the host-parasite relationship. For this reason it appears beneficial for the parasite to elicit in its host a Th2 response leading to tissue eosinophilia, during the muscle stage of infection.
  • #35 Trichinella inflammatory myopathy: host or parasite strategy? | Parasites & Vectors | Full Text
    https://parasitesandvectors.biomedcentral.com/articles/10.1186/1756-3305-4-42
    The immunological response to T. spiralis muscle invasion is mainly characterized by a Th2 phenotype, in fact cells collected from cervical lymph nodes of infected mice produce IL-5, IL-10, IL-13 and IFN- after stimulation with somatic larval antigens. […] In knock-out (KO) mice for the interleukin-10 (IL-10) gene (IL10-/-), the extent of the inflammatory infiltrate around the NC was markedly increased compared with control mice during the acute phase of infection, though the cellular composition remained the same. […] The role of eosinophils in experimental trichinellosis shows that muscle larvae are damaged by an immune response driven by Th1 cells which seem to be downregulated by eosinophils. […] Information derived from the studies on Trichinella-induced muscle inflammation provide new perspectives of the host-parasite relationship. For this reason it appears beneficial for the parasite to elicit in its host a Th2 response leading to tissue eosinophilia, during the muscle stage of infection.
  • #36 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The synthesis and release of IL-4 and IL-13 induce B cell proliferation and the expression of surface antigens, including the CD23 receptor (FcRII) of low affinity to IgE and MHC class II molecules, stimulating the production of IgE. […] Immunotherapy with T. spiralis TS antigen provoked a primary immune response, with a reduction in parasite burden, as well as damage to CN in the muscular phase of the infection. […] Thus, 45-kDa immunodominant antigen has been shown to be the most effective antigen against T. spiralis infection.
  • #37 Trichinosis | MedLink Neurology
    https://www.medlink.com/articles/trichinosis
    Mechanisms underlying vital organ involvement are still debated. Whether disseminated larvae alone or with an associated toxemia account for the damage to the internal organs has not yet been clearly demonstrated. A purely mechanical theory suggests that the larva cause the occlusion of small cerebral endarterioles, resulting in distal ischemia. […] However, although direct invasion of myocardium and brain parenchyma by T spiralis has been evident, larva encystment in these organs has been reported only rarely.
  • #38 Trichinosis | MedLink Neurology
    https://www.medlink.com/articles/trichinosis
    Mechanisms underlying vital organ involvement are still debated. Whether disseminated larvae alone or with an associated toxemia account for the damage to the internal organs has not yet been clearly demonstrated. A purely mechanical theory suggests that the larva cause the occlusion of small cerebral endarterioles, resulting in distal ischemia. […] However, although direct invasion of myocardium and brain parenchyma by T spiralis has been evident, larva encystment in these organs has been reported only rarely.
  • #39 Trichinosis complicated with hepatitis and myopericarditis
    https://www.oatext.com/Trichinosis-complicated-with-hepatitis-and-myopericarditis.php
    Trichinenosis also called trichinellosis is a parasitic infection caused by nematode helminthes of trichinella. This disease is a zoonosis that could be acquired when consuming of undercooked or raw meat or meat infected with trichinella larvae. The most common etiology is consumption of pork, but meat of other animals may cause the disease as well. […] The pathogenesis of the hepatic involvement is due to the penetration of the larvae to the hepatic sinusoids. This hepatic changes may be seen through or after the intestinal phase and could be attributed to direct injury (the larvae) or indirect injury (immunological or eosinophilia) and a long course of the disease might result in irreversible damage. […] These enzymes are released to the peripheral blood in greater amounts than their normal concentrations when there is a damage to the liver cell membrane resulting in higher permeability, same pathogenesis is believed to be caused by trichinilosis infection. […] To summarize, Trichinella infection is a multi-organ infiltrative disease despite the fact that little was reported in the recent years.
  • #40 Trichinosis complicated with hepatitis and myopericarditis
    https://www.oatext.com/Trichinosis-complicated-with-hepatitis-and-myopericarditis.php
    Trichinenosis also called trichinellosis is a parasitic infection caused by nematode helminthes of trichinella. This disease is a zoonosis that could be acquired when consuming of undercooked or raw meat or meat infected with trichinella larvae. The most common etiology is consumption of pork, but meat of other animals may cause the disease as well. […] The pathogenesis of the hepatic involvement is due to the penetration of the larvae to the hepatic sinusoids. This hepatic changes may be seen through or after the intestinal phase and could be attributed to direct injury (the larvae) or indirect injury (immunological or eosinophilia) and a long course of the disease might result in irreversible damage. […] These enzymes are released to the peripheral blood in greater amounts than their normal concentrations when there is a damage to the liver cell membrane resulting in higher permeability, same pathogenesis is believed to be caused by trichinilosis infection. […] To summarize, Trichinella infection is a multi-organ infiltrative disease despite the fact that little was reported in the recent years.
  • #41 Trichinosis complicated with hepatitis and myopericarditis
    https://www.oatext.com/Trichinosis-complicated-with-hepatitis-and-myopericarditis.php
    Trichinenosis also called trichinellosis is a parasitic infection caused by nematode helminthes of trichinella. This disease is a zoonosis that could be acquired when consuming of undercooked or raw meat or meat infected with trichinella larvae. The most common etiology is consumption of pork, but meat of other animals may cause the disease as well. […] The pathogenesis of the hepatic involvement is due to the penetration of the larvae to the hepatic sinusoids. This hepatic changes may be seen through or after the intestinal phase and could be attributed to direct injury (the larvae) or indirect injury (immunological or eosinophilia) and a long course of the disease might result in irreversible damage. […] These enzymes are released to the peripheral blood in greater amounts than their normal concentrations when there is a damage to the liver cell membrane resulting in higher permeability, same pathogenesis is believed to be caused by trichinilosis infection. […] To summarize, Trichinella infection is a multi-organ infiltrative disease despite the fact that little was reported in the recent years.
  • #42 Trichinellosis – Helminthiases – Parasitic Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.69.3.
    Depending on severity, invasion may be asymptomatic, subclinical, or associated with mild, moderate, or severe symptoms, including: […] Typical symptoms of trichinellosis, which are caused by penetration of larvae to muscle cells and a severe local inflammatory reaction: […] Signs and symptoms of parasitic tissue damage: Periorbital or (rarely) facial edema, petechiae in the conjunctiva and nail beds (in severe cases similar hemorrhages are also found in the brain, lungs, pericardium, and endocardium). […] In patients with severe trichinellosis (massive invasion) death can occur as a result of myocarditis, heart failure, meningitis, or encephalitis.
  • #43 Pathology of Trichinellosis (Trichinosis) – Dr Sampurna Roy MD
    http://www.histopathology-india.net/trichinosis.htm
    Trichinellosis, or trichinosis, is a parasitic zoonosis caused by nematodes of the genus Trichinella. […] Humans become infected by eating undercooked or raw meat containing encysted larvae, mainly pork. […] The cysts located in striated muscle, are digested, liberating larvae that mature to adult worms that attach to the wall of the small intestine. […] Female worms there liberate larvae that invade the intestinal wall, enter the circulation, and penetrate striated muscle, where they encyst and remain viable for years. […] On invasion of the muscle the larvae cause inflammation and destruction of muscle fibres. A fibrous hyaline layer develops around a single coiled larva. Histiocytes and giant cells may surround the cyst, which eventually calcifies. […] Larvae in other organs, including the heart and brain, cause edema, necrosis, and focal infiltration of neutrophils, eosinophils, and lymphocytes, but they do not encyst.
  • #44 Trichinellosis – Helminthiases – Parasitic Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.69.3.
    Depending on severity, invasion may be asymptomatic, subclinical, or associated with mild, moderate, or severe symptoms, including: […] Typical symptoms of trichinellosis, which are caused by penetration of larvae to muscle cells and a severe local inflammatory reaction: […] Signs and symptoms of parasitic tissue damage: Periorbital or (rarely) facial edema, petechiae in the conjunctiva and nail beds (in severe cases similar hemorrhages are also found in the brain, lungs, pericardium, and endocardium). […] In patients with severe trichinellosis (massive invasion) death can occur as a result of myocarditis, heart failure, meningitis, or encephalitis.
  • #45 Trichinellosis – Helminthiases – Parasitic Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.69.3.
    Depending on severity, invasion may be asymptomatic, subclinical, or associated with mild, moderate, or severe symptoms, including: […] Typical symptoms of trichinellosis, which are caused by penetration of larvae to muscle cells and a severe local inflammatory reaction: […] Signs and symptoms of parasitic tissue damage: Periorbital or (rarely) facial edema, petechiae in the conjunctiva and nail beds (in severe cases similar hemorrhages are also found in the brain, lungs, pericardium, and endocardium). […] In patients with severe trichinellosis (massive invasion) death can occur as a result of myocarditis, heart failure, meningitis, or encephalitis.
  • #46 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The NC formation process is a complex process and includes the cellular response of the infected muscle and the responses of the NC. […] This explains why CN seems intact and active for years despite intracellular parasitism. […] The main striated muscles where the L1-T. spiralis is implanted are the most active such as the diaphragm, masseters, intercostals, eye muscles, muscles of the tongue, and anterior and posterior extremities. […] The severity of the clinical disease is strongly dependent and directly correlated with the number of L1-T. spiralis ingested, age, sex, invaded tissue, nutritional, hormonal and immune status. […] The clinical pathology of Trichinellosis can be divided based on the phases of the T. spiralis life cycle. […] The Th1 type immune response against T. spiralis is characterized by a significant increase in Th1 cytokines such as IL-12, INF-, IL-1 and TNF-.
  • #47 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The NC formation process is a complex process and includes the cellular response of the infected muscle and the responses of the NC. […] This explains why CN seems intact and active for years despite intracellular parasitism. […] The main striated muscles where the L1-T. spiralis is implanted are the most active such as the diaphragm, masseters, intercostals, eye muscles, muscles of the tongue, and anterior and posterior extremities. […] The severity of the clinical disease is strongly dependent and directly correlated with the number of L1-T. spiralis ingested, age, sex, invaded tissue, nutritional, hormonal and immune status. […] The clinical pathology of Trichinellosis can be divided based on the phases of the T. spiralis life cycle. […] The Th1 type immune response against T. spiralis is characterized by a significant increase in Th1 cytokines such as IL-12, INF-, IL-1 and TNF-.
  • #48 Clinical Overview of Trichinellosis | Trichinellosis (Trichinosis) | CDC
    https://www.cdc.gov/trichinellosis/hcp/clinical-overview/index.html
    Trichinellosis is caused by infection with the parasite Trichinella. The severity of disease is related to the infectious dose and host characteristics, such as age of the patient or immunological priming as a result of previous Trichinella infection. […] Some reports have linked severity of disease to the infecting species of Trichinella, suggesting that certain species are more likely to cause severe disease than others. However, the pathogenicity of various species is difficult to define clinically without quantifying infectious dose. […] Digestion releases the parasite larvae from the meat, then larvae penetrate the intestinal mucosa where they mature into adult worms. The adult worms mate and produce new larvae, which migrate via the bloodstream to skeletal muscle throughout the body. The immune response leads to expulsion of the adult worms after several weeks, but the larvae, once in striated muscle cells, can persist for months or years.
  • #49 Clinical Overview of Trichinellosis | Trichinellosis (Trichinosis) | CDC
    https://www.cdc.gov/trichinellosis/hcp/clinical-overview/index.html
    Trichinellosis is caused by infection with the parasite Trichinella. The severity of disease is related to the infectious dose and host characteristics, such as age of the patient or immunological priming as a result of previous Trichinella infection. […] Some reports have linked severity of disease to the infecting species of Trichinella, suggesting that certain species are more likely to cause severe disease than others. However, the pathogenicity of various species is difficult to define clinically without quantifying infectious dose. […] Digestion releases the parasite larvae from the meat, then larvae penetrate the intestinal mucosa where they mature into adult worms. The adult worms mate and produce new larvae, which migrate via the bloodstream to skeletal muscle throughout the body. The immune response leads to expulsion of the adult worms after several weeks, but the larvae, once in striated muscle cells, can persist for months or years.
  • #50 CDC – DPDx – Trichinellosis
    https://www.cdc.gov/dpdx/trichinellosis/index.html
    Trichinellosis (trichinosis) is caused by nematodes (roundworms) of the genus Trichinella. […] Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T. pseudospiralis and T. papuae, which do not encyst) of Trichinella species. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms. […] Diagnosis is usually made based on clinical symptoms, and is confirmed by serology or identification of encysted or non-encysted larvae in biopsy or autopsy specimens. […] The suspicion of trichinellosis (trichinosis), based on history, clinical symptoms, and eosinophilia, can be confirmed by specific diagnostic tests, including antibody detection, muscle biopsy, and microscopy.
  • #51 Clinical Overview of Trichinellosis | Trichinellosis (Trichinosis) | CDC
    https://www.cdc.gov/trichinellosis/hcp/clinical-overview/index.html
    In addition to physical damage to affected tissues, larval penetration and tissue migration cause an immune-mediated inflammatory reaction and stimulate the development of eosinophilia. More severe manifestations include myocarditis, encephalitis, and thromboembolic disease. […] Muscle biopsies are infrequently performed, but they allow for the molecular identification of the Trichinella species or genotype, which is not possible with antibody testing. Usually, 0.2 to 0.5 grams of human or animal skeletal muscle tissue is collected and examined for Trichinella larvae via artificial digestion or histological analysis.
  • #52 CDC – DPDx – Trichinellosis
    https://www.cdc.gov/dpdx/trichinellosis/index.html
    Trichinellosis (trichinosis) is caused by nematodes (roundworms) of the genus Trichinella. […] Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T. pseudospiralis and T. papuae, which do not encyst) of Trichinella species. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms. […] Diagnosis is usually made based on clinical symptoms, and is confirmed by serology or identification of encysted or non-encysted larvae in biopsy or autopsy specimens. […] The suspicion of trichinellosis (trichinosis), based on history, clinical symptoms, and eosinophilia, can be confirmed by specific diagnostic tests, including antibody detection, muscle biopsy, and microscopy.
  • #53 Clinical Overview of Trichinellosis | Trichinellosis (Trichinosis) | CDC
    https://www.cdc.gov/trichinellosis/hcp/clinical-overview/index.html
    In addition to physical damage to affected tissues, larval penetration and tissue migration cause an immune-mediated inflammatory reaction and stimulate the development of eosinophilia. More severe manifestations include myocarditis, encephalitis, and thromboembolic disease. […] Muscle biopsies are infrequently performed, but they allow for the molecular identification of the Trichinella species or genotype, which is not possible with antibody testing. Usually, 0.2 to 0.5 grams of human or animal skeletal muscle tissue is collected and examined for Trichinella larvae via artificial digestion or histological analysis.
  • #54 Clinical Overview of Trichinellosis | Trichinellosis (Trichinosis) | CDC
    https://www.cdc.gov/trichinellosis/hcp/clinical-overview/index.html
    In addition to physical damage to affected tissues, larval penetration and tissue migration cause an immune-mediated inflammatory reaction and stimulate the development of eosinophilia. More severe manifestations include myocarditis, encephalitis, and thromboembolic disease. […] Muscle biopsies are infrequently performed, but they allow for the molecular identification of the Trichinella species or genotype, which is not possible with antibody testing. Usually, 0.2 to 0.5 grams of human or animal skeletal muscle tissue is collected and examined for Trichinella larvae via artificial digestion or histological analysis.
  • #55 Trichinosis – Infectious Diseases – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/infectious-diseases/nematodes-roundworms/trichinosis
    The Trichinella life cycle is maintained by animals that are fed (eg, pigs) or eat (eg, bears, foxes, boars) other animals whose striated muscles contain encysted infective larvae (eg, rodents). Humans become infected by eating undercooked meat from infected animals, most commonly pigs, wild boar, or bear. […] Larvae excyst in the small intestine, penetrate the mucosa, and become adults in 6 to 8 days. […] Mature females release living larvae for 4 to 6 weeks and then die or are expelled. Newborn larvae migrate through the bloodstream and lymphatics but ultimately survive only within striated skeletal muscle cells. Larvae fully encyst in 1 to 2 months and remain viable for several years as intracellular parasites. […] Anthelmintics eliminate adult Trichinella worms from the gastrointestinal tract, but once larvae encyst in skeletal muscle, treatment may not eradicate them or any associated symptoms. However, most people with trichinosis recover fully. […] The efficacy of higher doses and prolonged courses in killing encysted larvae is uncertain and adverse effects are more likely.
  • #56 Trichinosis Fact Sheet – MN Dept. of Health
    https://www.health.state.mn.us/diseases/trichinosis/trichinosis.html
    Trichinosis can be treated with safe and effective anti-parasitic drugs that are available by prescription. Treatment decisions should be made as early as possible, in consultation with medical experts. Mild cases can resolve on their own, but severe cases can be fatal without treatment. There is no treatment once the larvae are embedded in muscles.
  • #57 Trichinosis: Causes, symptoms, and treatment
    https://www.medicalnewstoday.com/articles/trichinosis
    Trichinosis, also known as trichinellosis, is an infection with a parasite called Trichinella. In humans, it starts in the stomach and small intestine. […] After a person ingests the parasites, the larvae enter the small intestine, where they mature and reproduce. The female worms then release larvae that migrate from the small intestine into the circulation to reach the muscles. Once in the muscles, the worms can live for an extended period. […] Treating trichinosis within the first 3 days of infection can prevent muscular invasion and disease progression. […] As Trichinella is a helminth (parasitic worm), a doctor will prescribe an antihelminthic drug, such as albendazole or mebendazole.
  • #58 Trichinosis Fact Sheet – MN Dept. of Health
    https://www.health.state.mn.us/diseases/trichinosis/trichinosis.html
    Trichinosis can be treated with safe and effective anti-parasitic drugs that are available by prescription. Treatment decisions should be made as early as possible, in consultation with medical experts. Mild cases can resolve on their own, but severe cases can be fatal without treatment. There is no treatment once the larvae are embedded in muscles.
  • #59 Trichinosis – Diagnosis & treatment – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/trichinosis/diagnosis-treatment/drc-20378587
    Trichinella larvae travel from the small intestine through your bloodstream to bury themselves inside muscle tissue. […] Anti-parasitic medication is the first line of treatment for trichinosis. If your provider discovers that you have roundworm (trichinella) parasites early, albendazole (Albenza) or mebendazole (Emverm) can kill the worms and larvae in the small intestine. […] If your provider discovers the infection after the larvae bury themselves in muscle tissues, the anti-parasitic drugs may not kill all the parasites. However, your provider might prescribe one if you have brain, heart or lung problems due to larvae causing pain and swelling (inflammation) in these organs. […] Sometimes trichinosis can cause an allergic reaction. This happens when the parasite enters muscle tissue or when dead or dying larvae release chemicals in your muscle tissue. Your provider might prescribe a steroid medication to control pain and swelling.
  • #60 Research progress on the immune evasion mechanism in Trichinella spiralis infection
    https://www.jsczz.cn/EN/Y2023/V41/I4/492
    Trichinella spiralis infection can cause zoonotic trichinellosis that seriously endangers human health. […] The immune evasion mechanism, as a common natural selection mechanism, is an adaptation of pathogens to the immune system under natural selection. It enables the pathogens to relieve or alleviate the host’s immune responses, avoid attacking from the immune system, and ensure that they can survive and reproduce. […] Further research of the immune evasion mechanism of Trichinella spiralis is of great significance for the prevention and control of trichinosis, the treatment of human autoimmune diseases, and allergic diseases.
  • #61 Research progress on the immune evasion mechanism in Trichinella spiralis infection
    https://www.jsczz.cn/EN/Y2023/V41/I4/492
    Trichinella spiralis infection can cause zoonotic trichinellosis that seriously endangers human health. […] The immune evasion mechanism, as a common natural selection mechanism, is an adaptation of pathogens to the immune system under natural selection. It enables the pathogens to relieve or alleviate the host’s immune responses, avoid attacking from the immune system, and ensure that they can survive and reproduce. […] Further research of the immune evasion mechanism of Trichinella spiralis is of great significance for the prevention and control of trichinosis, the treatment of human autoimmune diseases, and allergic diseases.
  • #62 Trichinella spiralis Infection – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK538511/
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] Enteric or gastrointestinal phase: After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Systemic (parenteral) phase: Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #63 Trichinella spiralis Infection | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/616
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #64 Trichinella spiralis Infection – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK538511/
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] Enteric or gastrointestinal phase: After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Systemic (parenteral) phase: Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #65 Trichinella spiralis Infection | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/616
    Ingestion of undercooked or raw meat from domestic or sylvatic animals containing encysted larvae of Trichinella species can lead to Trichinellosis. T. spiralis results from the consumption of inadequately cooked or raw pork from domestic pigs. […] After ingestion of infected meat by humans, the enzymes pepsin and hydrochloric acid act in the stomach and cause the release of the 1st stage of the larvae. These larvae invade the small intestine. Invasion can be asymptomatic or sometimes associated with abdominal pain, diarrhea, nausea, and vomiting. Larvae then turn into adults and mate. Female trichinella worms produce larvae, which completes the gastrointestinal or enteric phase. […] Larvae enter the lymphatic circulation and then into the blood, reaching skeletal muscles, myocardium, and brain which are high in oxygen content. This phase leads to systemic symptoms like fevers, myositis, myalgias, periorbital edema and can even cause myocarditis and encephalitis. […] The larvae provoke significant eosinophilia, especially in patients who develop cardiac and CNS dysfunction.
  • #66 A novel Trichinella spiralis serine proteinase disrupted gut epithelial barrier and mediated larval invasion through binding to RACK1 and activating MAPK/ERK1/2 pathway | PLOS Neglected Tropical Diseases
    https://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011872
    A novel Trichinella spiralis serine proteinase disrupted gut epithelial barrier and mediated larval invasion through binding to RACK1 and activating MAPK/ERK1/2 pathway. […] The aim of this study was to characterize the interacted proteins of TsSPc and IECs, and to investigate the molecular mechanisms of TsSPc mediating larval invasion of gut mucosa. […] rTsSPc bound to RACK1 receptor in gut epithelium, activated MAPK/ERK1/2 pathway, decreased the expression of gut epithelial TJs proteins and disrupted the epithelial integrity, consequently mediated T. spiralis larval invasion of gut epithelium. […] The results indicated that TsSPc binding to gut epithelial RACK1 receptor activated MAPK/ERK1/2 pathway, decreased expression of gut TJs proteins, and destroyed gut epithelial integrity, thereby mediated T. spiralis larval invasion of gut mucosa. […] The results demonstrated that rTsSPc binding to RACK1 receptor in Caco-2 cells activated ERK1/2 signaling pathway, reduced the expression of TJs proteins and damaged the integrity and barrier function of gut epithelium, consequently mediated the larval invasion of gut mucosa.
  • #67 Current Aspects in Trichinellosis | IntechOpen
    https://www.intechopen.com/chapters/63554
    The synthesis and release of IL-4 and IL-13 induce B cell proliferation and the expression of surface antigens, including the CD23 receptor (FcRII) of low affinity to IgE and MHC class II molecules, stimulating the production of IgE. […] Immunotherapy with T. spiralis TS antigen provoked a primary immune response, with a reduction in parasite burden, as well as damage to CN in the muscular phase of the infection. […] Thus, 45-kDa immunodominant antigen has been shown to be the most effective antigen against T. spiralis infection.