Katar sienny
Patofizjologia i mechanizm

Katar sienny, czyli sezonowy alergiczny nieżyt nosa, jest chorobą zapalną górnych dróg oddechowych, wynikającą z nadwrażliwości typu I na alergeny środowiskowe. Patogeneza obejmuje fazę wczesną, trwającą 2-3 godziny, z degranulacją komórek tucznych i uwalnianiem mediatorów takich jak histamina, leukotrieny i prostaglandyna D2, co prowadzi do objawów takich jak kichanie, świąd, obrzęk i przekrwienie błony śluzowej nosa. Faza późna, rozwijająca się 4-8 godzin po ekspozycji, charakteryzuje się przewlekłym zapaleniem z udziałem eozynofili, limfocytów T i bazofilów, utrzymującym przekrwienie i produkcję śluzu przez 18-24 godziny. Lokalna produkcja IgE w błonie śluzowej nosa oraz ekspresja receptorów FcεRI na komórkach tucznych wzmacniają reakcję alergiczną. W patogenezie istotną rolę odgrywają cytokiny Th2 (IL-4, IL-5, IL-13), eotaksyna, a także czynniki takie jak TSLP, IL-25 i IL-33, które aktywują komórki ILC2 i nasilają odpowiedź zapalną. Genetyczne predyspozycje, epigenetyka oraz dysbioza mikrobiomu jelitowego wpływają na rozwój i przebieg choroby, a zmiany klimatyczne i zanieczyszczenie powietrza nasilają objawy alergiczne.

Patogeneza kataru siennego

Katar sienny, znany również jako alergiczny nieżyt nosa o charakterze sezonowym, jest złożoną chorobą zapalną górnych dróg oddechowych, która ma znaczący wpływ na jakość życia pacjentów i stanowi obciążenie społeczno-ekonomiczne. Jest wynikiem nieprawidłowej reakcji immunologicznej na alergeny obecne w środowisku, które u większości osób nie wywołują żadnych objawów.12

Proces uczulenia i klasyfikacja reakcji alergicznej

Katar sienny klasyfikowany jest jako reakcja nadwrażliwości typu I. Proces uczulenia (sensytyzacji) rozpoczyna się, gdy alergen przenika przez barierę błony śluzowej nosa. Bariera ta może być bardziej przepuszczalna u osób predysponowanych do alergii. Następnie alergen jest pochłaniany przez komórkę prezentującą antygen (APC), taką jak komórka dendrytyczna, która prezentuje go naiwnym limfocytom T CD4+, stymulując ich różnicowanie w kierunku limfocytów pomocniczych Th2.34

Limfocyty Th2 wydzielają cytokiny prozapalne, w tym IL-4, IL-5, IL-13, IL-14 i IL-31. Te cytokiny z kolei stymulują limfocyty B do różnicowania się w komórki plazmatyczne i uwalniania specyficznych dla alergenu przeciwciał IgE. Przeciwciała te przyłączają się do receptorów FcεRI na powierzchni komórek tucznych w błonie śluzowej nosa oraz bazofilów we krwi obwodowej. Cytokiny prozapalne rekrutują również inne komórki zapalne, takie jak bazofile, eozynofile i fibroblasty do obszaru zapalenia.56

Faza wczesna reakcji alergicznej

Wczesna faza reakcji alergicznej pojawia się u uczulonych osób w ciągu minut od ekspozycji na alergen i trwa około 2-3 godzin. Kluczowym elementem tej fazy jest degranulacja komórek tucznych.7

Gdy osoba uczulona ponownie napotka ten sam alergen, dochodzi do jego wiązania z przeciwciałami IgE znajdującymi się na powierzchni komórek tucznych, co prowadzi do ich aktywacji. Komórki tuczne uwalniają preformowane mediatory zapalne, takie jak:89

  • Histamina – główny mediator naczyniowy, powodujący rozszerzenie naczyń, zwiększoną przepuszczalność naczyń i stymulację nerwów czuciowych
  • Tryptaza
  • Chymaza
  • Kininy
  • Heparyna

10

Komórki tuczne szybko syntetyzują również inne mediatory, w tym leukotrieny i prostaglandynę D2. Te mediatory, poprzez różne interakcje, prowadzą ostatecznie do objawów takich jak kichanie, swędzenie, zaczerwienienie, łzawienie, obrzęk, uczucie zatkania uszu, spływanie wydzieliny po tylnej ścianie gardła.11

Histamina działając na receptory H1 na nerwach czuciowych powoduje rozszerzenie naczyń i zwiększoną przepuszczalność osocza. Stymulacja włókien nerwów przywspółczulnych (cholinergicznych) przez leukotrieny i inne mediatory powoduje wydzielanie śluzu z gruczołów nosowych. Leukotrieny zwiększają również przepuszczalność naczyń. Skutkiem jest wyciek z nosa i przekrwienie, które osiągają maksimum po 15-30 minutach.12

Faza późna reakcji alergicznej

Faza późna rozwija się w ciągu 4-8 godzin po ekspozycji na alergen i charakteryzuje się przedłużeniem objawów – kichaniem, wyciekiem z nosa, ale przede wszystkim utrzymującym się przekrwieniem nosa, które trwa około 18-24 godzin.1314

Ta faza ma charakter głównie zapalny i charakteryzuje się napływem komórek zapalnych, takich jak limfocyty T, bazofile, neutrofile, eozynofile i makrofagi do błony śluzowej. Prowadzi to do dalszego zapalenia, stąd nazwa „odpowiedź późnej fazy”.1516

Uwalniane są różne mediatory, w tym leukotrieny, kininy i histamina, które powodują kontynuację objawów i rozwój fazy późnej. Komórki tuczne uwalniają również cytokiny, takie jak IL-4 i IL-13, które mogą zwiększać ekspresję „cząsteczek adhezyjnych”, takich jak cząsteczka adhezji komórkowej naczyń 1 (VCAM-1) na komórkach śródbłonka, ułatwiając infiltrację eozynofili, limfocytów T i bazofili do błony śluzowej nosa.17

Objawy późnej fazy są podobne do objawów fazy wczesnej, ale występuje mniej kichania i świądu, a więcej przekrwienia i produkcji śluzu. Faza późna może utrzymywać się przez godziny lub dni.18

Przewlekłe zapalenie i przebudowa tkanek

Trwająca, przedłużona ekspozycja na alergen i powtarzające się odpowiedzi późnej fazy prowadzą do postępującego zapalenia błony śluzowej nosa i zwiększonej wrażliwości na alergeny. Ilość alergenu zdolna do wywołania reakcji alergicznej zmniejsza się z czasem, efekt określany jako torowanie (priming). Efekt torowania tłumaczy rozwój nadreaktywności błony śluzowej na bodźce niealergenowe, takie jak silne zapachy, dym papierosowy i niskie temperatury.19

W wyniku zapalenia błony śluzowej tkanki zostają uwrażliwione i reagują bardziej intensywnie na ekspozycję na alergen. Ciężki katar sienny może zwiększyć prawdopodobieństwo rozwoju innych schorzeń, takich jak zapalenie zatok przynosowych. Katar sienny często sprawia również, że błony śluzowe wyściełające drogi oddechowe stają się ogólnie nadwrażliwe. W rezultacie mogą one również silniej reagować na inne czynniki drażniące, takie jak suche powietrze w ogrzewanych pomieszczeniach czy dym papierosowy.20

Istnieją dowody na trwające zapalenie w drogach oddechowych nawet wtedy, gdy objawy nieżytu nosa lub astmy są spokojne, co wskazuje na stałą aktywność procesów zapalnych.21

Kluczowe komórki w patogenezie kataru siennego

Komórki tuczne

Komórki tuczne odgrywają centralną rolę w mechanizmach immunologicznych alergicznego nieżytu nosa. U pacjentów z alergicznym nieżytem nosa komórki tuczne gromadzą się obficie w przedziale nabłonkowym błony śluzowej nosa i są to przeważnie komórki o fenotypie MC(T).22

Komórki tuczne indukują również syntezę IgE w komórkach B i odgrywają kluczową rolę poprzez kaskadę receptor IgE-IgE komórki tucznej. Lokalne wytwarzanie IgE w błonie śluzowej nosa jest obecnie dobrze udokumentowane. Lokalnie wytwarzane IgE może następnie odgrywać kluczową rolę w wzmacnianiu aktywności komórek tucznych poprzez zwiększanie ekspresji FcεRI w komórkach tucznych i późniejsze uwalnianie mediatorów po skrzyżowaniu związanego IgE.2324

Eozynofile

Eozynofile odgrywają istotną rolę w przewlekłych chorobach alergicznych, co czyni je głównymi celami badań podstawowych i terapeutycznych. Eotaksyna wydaje się być kluczowa dla dojrzewania i uwalniania eozynofili ze szpiku kostnego.25

W tkankach cytokiny takie jak IL-5 i GM-SCF utrzymują eozynofile przy życiu przez kilka dni, a nawet tygodni, co pozwala przezwyciężyć zaprogramowaną śmierć komórki (apoptozę). Istnieje znacząca korelacja między wzrostem liczby limfocytów T CD4+ podczas późnej fazy reakcji alergicznej po prowokacji alergenem a liczbą infiltrujących eozynofili w błonie śluzowej.2627

Limfocyty T

Limfocyty T są jednymi z głównych czynników regulujących i koordynujących odpowiedzi immunologiczne w chorobach alergicznych. Zapalenie błony śluzowej w alergicznym nieżycie nosa charakteryzuje się infiltracją tkanki przez limfocyty T (komórki T CD4+ i CD25+ (aktywowane) komórki T) zarówno w podśluzówce, jak i nabłonku.28

Ligand dla chemokiny TARC, CCR4, okazał się być ekspresjonowany przez komórki Th2. W alergicznym nieżycie nosa występuje zaburzenie równowagi między komórkami promującymi alergię Th2 a komórkami Th1 zwalczającymi infekcje.2930

W szczególności u osób z alergicznym nieżytem nosa obserwuje się ekspansję nowo zróżnicowanych komórek pomocniczych typu 2 (Th2) i istniejących pamięciowych komórek Th2 w płucach. Te komórki mogą wytwarzać chemiczne substancje, które sygnalizują eozynofilom i mogą pomóc wywołać astmę i zapalenie dróg oddechowych.31

Komórki dendrytyczne i makrofagi

Reakcje alergiczne występują w środowisku śluzówki, które jest bogate zarówno w komórki dendrytyczne, jak i makrofagi. Istnieją jednak znaczące różnice między dolnymi a górnymi drogami oddechowymi, ponieważ makrofagi pęcherzykowe stanowią ponad 90% populacji komórek w popłuczynach oskrzelowo-pęcherzykowych, ale makrofagi dróg oddechowych na powierzchni nabłonka nosa stanowią tylko około 1-2% komórek.32

Nowe mechanizmy i czynniki patogenetyczne

Cytokiny pochodzące z komórek nabłonka

Obecnie wiadomo, że alergeny, ze względu na swoją enzymatyczną aktywność proteolityczną, mogą bezpośrednio aktywować komórki. Uszkodzenie bariery nabłonkowej błony śluzowej nosa może również uwalniać alarminy (rodzaj cząsteczek wzorca molekularnego związanego z uszkodzeniem (DAMP)), takie jak limfopoetyna zrębu grasicy (TSLP), IL-25 i IL-33, które aktywują komórki limfoidalne wrodzone grupy 2 (ILC2), które następnie również uwalniają cytokiny zapalne prowadzące do aktywacji komórek odpornościowych.3334

Nabłonkowa TSLP pochodząca z komórek nabłonka jest głównym przełącznikiem dla astmy lub atopowego zapalenia skóry, indukując zapalenie alergiczne typu Th2 mediowane przez komórki dendrytyczne.35

Specyficzne warianty genów, które zmieniają kodowanie cytokin pochodzących z komórek nabłonka, takich jak interleukina-33 i limfopoetyna zrębu grasicy, mogą być zaangażowane w patogenezę alergii.36

Lokalna produkcja IgE

Produkcja IgE lokalnie w błonie śluzowej nosa jest obecnie dobrze udokumentowana. Lokalnie produkowane IgE może następnie odgrywać kluczową rolę w wzmacnianiu aktywności komórek tucznych poprzez zwiększanie ekspresji FcεRI w komórkach tucznych i późniejsze uwalnianie mediatorów po połączeniu związanego IgE z alergenem.3738

Interakcje neuro-immunologiczne

Czynnik wzrostu nerwów (NGF), który jest nadmiernie ekspresjonowany w alergicznym nieżycie nosa, jest związany z rozwojem nadreaktywności i jest również związany z zapaleniem alergicznym, moszcząc tym samym lukę między tymi dwiema cechami alergicznego nieżytu nosa i astmy.39

Osoby z alergiami prezentują objawy, które często są wynikiem zmian w układzie nerwowym. Istnieje wyraźny związek między objawami układu przywspółczulnego a alergicznym nieżytem nosa, ponieważ wyniki badań wskazują, że pacjenci z przerywanym i łagodnym alergicznym nieżytem nosa mają aktywność hiperwagalną i hiposympatyczną, a dominacja zmniejsza się u pacjentów z bardziej przewlekłym alergicznym nieżytem nosa i ciężkimi objawami.40

Ogólnoustrojowe zapalenie

Alergiczny nieżyt nosa nie jest związany tylko z miejscowym zapaleniem błony śluzowej nosa, ale ma również element ogólnoustrojowy. Zarówno alergiczny nieżyt nosa, jak i astma są chorobami zapalnymi, a ich mechanizmy zapalne są podobne, charakteryzując się naciekiem zapalnym złożonym z eozynofili, komórek T i komórek tucznych, które uwalniają kilka mediatorów, chemokin i cytokin, lokalną i ogólnoustrojową syntezą IgE oraz ogólnoustrojowym połączeniem poprzez szpik kostny.4142

Skuteczne zarządzanie tym przewlekłym alergicznym zespołem oddechowym wymaga zintegrowanego spojrzenia na drogi oddechowe, zrozumienia ich interakcji i zintegrowanego podejścia do leczenia, które również celuje w ogólnoustrojowe zapalenie.43

Czynniki genetyczne i epigenetyczne

Dziedziczenie i polimorfizmy genetyczne

Ekspresja chorób alergicznych górnych dróg oddechowych odzwierciedla autosomalny dominujący wzór dziedziczenia z niepełną penetracją. Ten wzór dziedziczenia przejawia się jako skłonność do reagowania na ekspozycję na alergen wziewny poprzez produkcję wysokich poziomów specyficznego dla alergenu IgE. Odpowiedź IgE wydaje się być kontrolowana przez geny odpowiedzi immunologicznej zlokalizowane w głównym kompleksie zgodności tkankowej (MHC) na chromosomie 6.44

Badania genomiczne wykazały związek genetyczny dotyczący patogenezy alergicznego nieżytu nosa. Według szacunków, katar sienny ma wysoki komponent dziedziczny, z indeksem dziedziczności wynoszącym 0,65. Kilka doniesień połączyło loci genetyczne i geny kandydujące z alergicznym nieżytem nosa. Różne geny przyczynowe alergicznego nieżytu nosa (np. SDAD1, CXCL10 i CXCL9) okazały się być związane z szeregiem zaburzeń związanych z układem odpornościowym.45

Te geny wpływają na wspólne genetyczne warianty ryzyka dla chorób atopowych, co sugeruje, że mogą one wykazywać typowe cechy patogenne i być wykorzystane do tworzenia nowych metod leczenia.46

Epigenetyka

Badania epigenetyczne alergicznego nieżytu nosa koncentrowały się na kilku kluczowych aspektach, obejmujących regulację ekspresji genów, metylację DNA, modyfikacje histonów i rolę niekodujących RNA. Badania wykazały korelację między ilością i wzorem komórek CD4+T w alergicznym nieżycie nosa a wzorem metylacji DNA, który może być wykorzystany do różnicowania pacjentów alergicznych od zdrowych osób.47

Metylacja DNA jest zaangażowana w postęp i skuteczność terapeutyczną alergicznego nieżytu nosa na wiele sposobów. Metabolomika koncentruje się na odkrywaniu nowych biomarkerów i monitorowaniu efektów terapeutycznych.48

Mikrobiom

Mikrobiom, często określany jako drugi ludzki genom, odnosi się do składu, funkcji i interakcji społeczności mikrobów gospodarza, która jest głównym składnikiem układu odpornościowego. Coraz więcej dowodów sugeruje, że pacjenci z chorobami alergicznymi, takimi jak astma, alergia pokarmowa, atopowe zapalenie skóry i alergiczny nieżyt nosa, mają dysbiozę mikrobioty jelitowej.49

Wykazano, że niektóre bakterie w mikrobiocie specyficznie blokują odpowiedzi immunologiczne zaangażowane w reakcje alergiczne. Nierównowaga w różnorodności mikrobioty danej osoby może sprzyjać odpowiedziom alergicznym.50

Czynniki środowiskowe

Zmiany klimatyczne i zanieczyszczenie powietrza

Wraz z pogarszaniem się zmian klimatycznych, pogarszają się również objawy alergiczne. Coraz częściej pracownicy służby zdrowia dochodzą do wniosku, że wraz ze wzrostem globalnego ciepła, rosną również objawy alergiczne.51

Badania zarówno w warunkach naturalnych, jak i laboratoryjnych wykazały, że większa wilgotność i wyższe poziomy dwutlenku węgla – który jest znanym stymulatorem wzrostu i reprodukcji roślin – zwiększają rozprzestrzenianie się alergennego pyłku. Globalne ocieplenie zaostrza również ekstremalne zjawiska pogodowe, takie jak huragany i powodzie, które zwiększają ryzyko rozwoju pleśni, powszechnego alergenu środowiskowego.52

Przypadki kataru siennego rosną ze względu na zmiany klimatyczne, ponieważ cieplejsza i bardziej wietrzna pogoda pomaga pyłkom podróżować dalej i pozostawać dłużej w powietrzu. Rosnące zanieczyszczenie powietrza jest również główną przyczyną. Katar sienny i astma alergiczna są często znacznie gorsze na przykład u dzieci dorastających w centrach miast lub na obszarach zabudowanych z dużą liczbą autostrad ze względu na zanieczyszczenie.5354

Hipoteza higieniczna

Hipoteza „Higieny”, czyli idea, że zwiększona ekspozycja na mikroorganizmy koreluje ze zmniejszoną tendencją do rozwoju alergii, jest jednym z wyjaśnień wzrostu częstości występowania.55

Hipoteza higieniczna sugeruje, że alergie pochodzą z nadreaktywnych i znudzonych układów odpornościowych bez wystarczającej ilości ekspozycji na bakterie, grzyby i pasożyty. Zakłada ona, że wraz z większym skupieniem świata na higienie, ludzie napotykali mniej zarazków i pasożytów. Ten brak stymulacji dla układu odpornościowego doprowadził do dysfunkcyjnego zachowania białych krwinek – zwłaszcza eozynofili, które bronią przed infekcjami pasożytniczymi, które nie są już tak powszechne.56

Nowe i nieoczekiwane ustalenia u myszy kwestionują jednak powszechną teorię, która łączy postrzegany wzrost alergii i astmy z pojawieniem się nowoczesnej higieny. Po wychowaniu myszy laboratoryjnych w półnaturalnych warunkach z dużą ilością mikrobów, badacze stwierdzili, że „zdziczałe” myszy nadal silnie reagowały na testy prowokacyjne alergenami. Te zaskakujące wyniki pokazują, że relacja między mikrobiotą a układem odpornościowym jest bardziej skomplikowana niż rozumiano.57

Implikacje dla leczenia

Celowanie w luki patofizjologiczne

Profile farmakologiczne dostępnych metod leczenia alergicznego nieżytu nosa pokazują, że istnieje szereg luk patofizjologicznych w farmakopei alergicznego nieżytu nosa. Żadna pojedyncza klasa leków nie jest w stanie zapewnić szybkiej i całkowitej ulgi od wszystkich objawów związanych z alergicznym nieżytem nosa.58

Profil farmakologiczny dostępnych metod leczenia alergicznego nieżytu nosa pokazuje, że istnieje kilka luk patofizjologicznych w farmakopei alergicznego nieżytu nosa. Jedna z nowych opcji terapeutycznych, MP-AzeFlu, składa się z wewnątrznosowego leku antyhistaminowego (AZE), wewnątrznosowego kortykosteroidu (FP) i nowatorskiej formulacji w pojedynczym sprayu. Oferuje on zatem korzyści wynikające z szerokiego pokrycia patofizjologicznego dzięki włączeniu dwóch środków z różnych klas leków o różnych, ale uzupełniających się mechanizmach działania, antagonizuje zarówno wczesne, jak i późne fazy reakcji alergicznych i jest wygodny w użyciu.59

Immunoterapia

Specyficzna immunoterapia alergenowa (znana również jako odczulanie) może zmniejszyć wrażliwość na alergeny w długim okresie. Podobnie jak w przypadku szczepionek, to podejście terapeutyczne polega na eksponowaniu ludzi na małe ilości alergenu. Odbywa się to w regularnych odstępach czasu przez wstrzykiwanie alergenu pod skórę lub umieszczanie go pod językiem. Specyficzna immunoterapia alergenowa trwa co najmniej trzy do pięciu lat.60

Immunoterapia powinna być rozważana w przypadku umiarkowanego lub ciężkiego przewlekłego alergicznego nieżytu nosa, który nie reaguje na zwykłe metody leczenia, u pacjentów, którzy nie tolerują standardowych terapii lub którzy chcą unikać długotrwałego stosowania leków, oraz u pacjentów z astmą alergiczną. Ukierunkowana immunoterapia, jedyna metoda leczenia, która zmienia naturalny przebieg alergicznego nieżytu nosa, polega na podawaniu małej ilości ekstraktu alergenu podskórnie lub podjęzykowo.61

Podczas AIT odpowiedzi układu odpornościowego ulegają zmianie. Zmiany te mogą obejmować produkcję mniejszej ilości IgE, produkcję „blokujących” przeciwciał IgG oraz produkcję większej liczby regulatorowych komórek T, promując tolerancję i mniej aktywną odpowiedź immunologiczną. Jednak dokładny mechanizm stojący za odczulaniem nie jest jeszcze znany i prawdopodobnie różni pacjenci wykazują różne profile immunologiczne po leczeniu.62

W immunoterapii podajemy pacjentowi zwiększające się dawki odpowiedniego ekstraktu pyłków w zależności od diagnozy (pyłki drzew, traw itp.). Możemy wpłynąć na źródło problemu i wytrenować organizm, aby przestał reagować na alergeny, bez ingerencji w inne części układu odpornościowego. Choć nie jest to lekarstwo, immunoterapia modyfikuje proces chorobowy, dzięki czemu wielu pacjentów może czuć, jakby nie mieli już kataru siennego.63

Nowe podejścia

Terapia z zastosowaniem taśm kinesiology w przypadku kataru siennego opiera się na zasadzie, że zewnętrzna stymulacja skóry może mieć odbicie oddziałujące na struktury tkankowe segmentów rdzenia kręgowego należących do obszaru unerwienia. Metoda leczenia taśmami polega na segmentalnym wsparciu przez grzbietową taśmę pleców nakładaną na obszar płuc. Możliwe wyjaśnienie zmniejszenia dolegliwości można znaleźć w uspokajającym działaniu na mechanizm reakcji alergicznej. Układ współczulny uspokaja się.64

Powięź zawiera wiele czujników. Nakładając taśmę na skórę, dostarczasz bodźca sensorycznego do powięzi, co tworzy inne napięcie; tkanka łączna uspokaja się. To z kolei ma pozytywny wpływ na układ odpornościowy, zmniejszając odpowiedź organizmu na katar sienny i tworzenie substancji do reakcji alergicznej. Prawdopodobnie napięcie powięzi i/lub stymulacja czujników w skórze ma pozytywny wpływ na wpływ immunoglobuliny IgE, a tym samym pośrednio na uwalnianie histaminy.65

Konwencjonalne leczenie kataru siennego obejmuje nieuspokajające leki przeciwhistaminowe i steroidy donosowe, które są zwykle dość skuteczne. Niektóre homeopatyczne metody leczenia wykazują obiecujące wyniki, przy czym kilka małych badań ma pozytywne wyniki przy użyciu ziół leczniczych do leczenia objawów alergii. Inne obiecujące naturalne środki obejmują akupunkturę i immunoterapię podjęzykową (SLIT), alternatywę dla zastrzyków, gdzie substancja alergiczna jest umieszczana pod językiem.6667

Obecne badania mają na celu znalezienie leków, które celują w określone etapy kaskady alergicznej, co może prowadzić do bardziej ukierunkowanych i skutecznych terapii w przyszłości.68

Kolejne rozdziały

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Wybierz kolejny rozdział z menu poniżej, aby otworzyć nową podstronę kompedium wiedzy i uzyskać szczegółowe informację o leku, substancji lub chorobie.

  1. 12.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Allergic rhinitis a chronic inflammatory disease of the upper airways that has a major impact on the quality of life of patients and is a socio-economic burden. Understanding the underlying immune mechanisms is central to developing better and more targeted therapies. The inflammatory response in the nasal mucosa includes an immediate IgE-mediated mast cell response as well as a late-phase response characterized by recruitment of eosinophils, basophils, and T cells expressing Th2 cytokines including interleukin (IL)-4, a switch factor for IgE synthesis, and IL-5, an eosinophil growth factor and on-going allergic inflammation. […] Recent advances have suggested new pathways like local synthesis of IgE, the IgE-IgE receptor mast cell cascade in on-going allergic inflammation and the epithelial expression of cytokines that regulate Th2 cytokine responses (i.e., thymic stromal lymphopoietin, IL-25, and IL-33).
  • #2 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. This barrier may be more permeable in susceptible individuals. The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31. These inflammatory cytokines stimulate B cells to differentiate into plasma cells and release allergen specific IgE immunoglobulins. The IgE immunoglobulins attach to mast cells. The inflammatory cytokines also recruit inflammatory cells such as basophils, eosinophils and fibroblasts to the area. The person is now sensitized, and upon re-exposure to the allergen, mast cells with allergen specific IgE will bind the allergens and release inflammatory molecules including histamine, leukotrienes, platelet activating factor, prostaglandins and thromboxane with these inflammatory molecules’ local effects on blood vessels (dilation), mucous glands (secrete mucous) and sensory nerves (activation) leading to the clinical signs and symptoms of allergic rhinitis.
  • #3 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. This barrier may be more permeable in susceptible individuals. The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31. These inflammatory cytokines stimulate B cells to differentiate into plasma cells and release allergen specific IgE immunoglobulins. The IgE immunoglobulins attach to mast cells. The inflammatory cytokines also recruit inflammatory cells such as basophils, eosinophils and fibroblasts to the area. The person is now sensitized, and upon re-exposure to the allergen, mast cells with allergen specific IgE will bind the allergens and release inflammatory molecules including histamine, leukotrienes, platelet activating factor, prostaglandins and thromboxane with these inflammatory molecules’ local effects on blood vessels (dilation), mucous glands (secrete mucous) and sensory nerves (activation) leading to the clinical signs and symptoms of allergic rhinitis.
  • #4 Pathogenesis of allergic diseases and implications for therapeutic interventions | Signal Transduction and Targeted Therapy
    https://www.nature.com/articles/s41392-023-01344-4
    Allergic diseases such as allergic rhinitis (AR), allergic asthma (AAS), atopic dermatitis (AD), food allergy (FA), and eczema are systemic diseases caused by an impaired immune system. […] The pathogenesis of allergic diseases is complex and involves many factors, including maternal-fetal environment, living environment, genetics, epigenetics, and the body’s immune status. […] The pathogenesis of allergic diseases exhibits a marked heterogeneity, with phenotype and endotype defining visible features and associated molecular mechanisms, respectively. […] The pathogenesis of AD is mainly reflected by a complex interplay between epidermal barrier dysfunction, abnormal skin microbiota and dysregulated type 2 T cell immunity. […] FA is an IgE-dependent type I hypersensitivity to a specific food allergen.
  • #5 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. It is classified as a type I hypersensitivity reaction. […] The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. […] The pathophysiology of allergic rhinitis involves Th2 Helper T cell and IgE mediated inflammation with overactive function of the adaptive and innate immune systems. The process begins when an aeroallergen penetrates the nasal mucosal barrier. This barrier may be more permeable in susceptible individuals. The allergen is then engulfed by an antigen presenting cell (APC) (such as a dendritic cell). The APC then presents the antigen to a Naive CD4+ helper T cell stimulating it to differentiate into a Th2 helper T cell. The Th2 helper T cell then secretes inflammatory cytokines including IL-4, IL-5, IL-13, IL-14, and IL-31. These inflammatory cytokines stimulate B cells to differentiate into plasma cells and release allergen specific IgE immunoglobulins. The IgE immunoglobulins attach to mast cells. The inflammatory cytokines also recruit inflammatory cells such as basophils, eosinophils and fibroblasts to the area. The person is now sensitized, and upon re-exposure to the allergen, mast cells with allergen specific IgE will bind the allergens and release inflammatory molecules including histamine, leukotrienes, platelet activating factor, prostaglandins and thromboxane with these inflammatory molecules’ local effects on blood vessels (dilation), mucous glands (secrete mucous) and sensory nerves (activation) leading to the clinical signs and symptoms of allergic rhinitis.
  • #6 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/134825-overview
    Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx. The nose invariably is involved, and the other organs are affected in certain individuals. Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin E (IgE)-mediated response to an extrinsic protein. […] The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins capable of causing an allergic reaction) has a genetic component. In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins. This specific IgE coats the surface of mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific pollen grain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to immediate and delayed release of a number of mediators.
  • #7 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Allergic rhinitis is an IgE-mediated inflammatory disease of the nasal mucous membranes due to the interaction of allergen characterized by an inflammatory infiltrate made up of eosinophils, T cells, mast cells and basophils, which release several mediators, chemokines and cytokines (among these, histamine and cysteinyl-leukotrienes are the major vasoactive mediators), regulation of the local and systemic IgE synthesis, and communication with the immune system and the bone marrow. […] The early or immediate phase response occurs in sensitized individuals within min of exposure to the allergen and lasts for about 2-3 h. One of the cardinal components of the early phase response is the degranulation of mast cells. […] The late phase response is characterized by a prolongation of symptoms – sneezing, rhinorrhea but most predominantly a sustained nasal congestion which lasts for about 18-24 h. The late phase response is predominantly inflammatory in nature and is characterized by a inflammatory cellular influx comprising of predominantly T lymphocytes, basophils and eosinophils.
  • #8 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/134825-overview
    The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction. […] Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days. […] Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
  • #9 Types of Allergies – Global Allergy & Airways Patient PlatformExpandExpandExpandExpandExpandExpandToggle MenuScroll to topScroll to topExpandExpandExpandExpandExpandExpand
    https://gaapp.org/diseases/allergies/types-of-allergies
    Allergies are classified into IgE mediated and non-IgE mediated allergies. […] In IgE mediated allergy the immune system produces great amounts of a class of antibodies known as IgE antibodies that are, specific for the particular offending allergen. […] These IgE antibodies bind to the surface of cells in the body called “mast cells” which become IgE-sensitized. […] The next time that we get in contact with the same allergen the mast cells identify it as an enemy and produce histamine and other chemicals. […] The release of these substances from mast cells induces the allergic symptoms. […] In the respiratory tract for example, these include sneezing, edema and mucus secretion, with vasodilatation in the nose, leading to nasal blockage, and bronchoconstriction in the lung, leading to wheezing.
  • #10 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    A variety of mediators are released by these cells including leukotrienes, kinins, histamine which result in the continuation of the symptoms and the development of the late phase. […] The key to the orchestration of the late phase response lies in the production and release of a variety of cytokines and chemokines like IL-4, IL-13 from mast cells as these cytokines can upregulate the expression of 'adhesion molecules’ like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. […] Mast cells play a central role in the immune mechanisms of allergic rhinitis. […] In patients with allergic rhinitis mast cells are found to abundantly accumulate in the epithelial compartment of the nasal mucosa and these are predominantly of the MC (T) phenotype.
  • #11 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/134825-overview
    The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction. […] Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days. […] Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
  • #12 Treatments for Seasonal Allergic Rhinitis | Effective Health Care (EHC) Program
    https://effectivehealthcare.ahrq.gov/products/allergy-seasonal/research-protocol
    Seasonal allergic rhinitis (SAR), also known as hay fever, is an inflammatory condition of the upper airways that occurs in response to exposure to airborne allergens (typically tree, grass, and weed pollens) in sensitized individuals. […] SAR results from the binding of an inhaled aeroallergen to immunoglobulin E (IgE) on the surface of mast cells in the nasal mucosa. An early phase allergic response follows: Mast cell degranulation releases preformed inflammatory mediators, such as histamine and leukotrienes, which produce immediate nasal itching and sneezing. Histamine stimulation of the histamine-1 (H1) receptors on sensory nerves causes vascular dilation and increased plasma leakage. Stimulation of parasympathetic (cholinergic) nerve fibers by leukotrienes and other mediators causes mucus secretion from nasal glands. Leukotrienes also increase vascular permeability. The result is nasal discharge and congestion, which is maximal at 15 to 30 minutes. Four to 12 hours after allergen exposure, a late-phase allergic response may occur. The late-phase response consists primarily of nasal congestion and is mediated by the influx and activation of inflammatory T-cells and eosinophils.
  • #13 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Allergic rhinitis is an IgE-mediated inflammatory disease of the nasal mucous membranes due to the interaction of allergen characterized by an inflammatory infiltrate made up of eosinophils, T cells, mast cells and basophils, which release several mediators, chemokines and cytokines (among these, histamine and cysteinyl-leukotrienes are the major vasoactive mediators), regulation of the local and systemic IgE synthesis, and communication with the immune system and the bone marrow. […] The early or immediate phase response occurs in sensitized individuals within min of exposure to the allergen and lasts for about 2-3 h. One of the cardinal components of the early phase response is the degranulation of mast cells. […] The late phase response is characterized by a prolongation of symptoms – sneezing, rhinorrhea but most predominantly a sustained nasal congestion which lasts for about 18-24 h. The late phase response is predominantly inflammatory in nature and is characterized by a inflammatory cellular influx comprising of predominantly T lymphocytes, basophils and eosinophils.
  • #14 Allergic Rhinitis: Symptoms and Treatment | Doctor
    https://patient.info/doctor/allergic-rhinitis-pro
    Allergic rhinitis is a common condition characterised by an immunoglobulin E (IgE)-mediated inflammation of the nasal mucosa following exposure to allergens. This gives rise to a release of preformed mediators (of which histamine appears to be the most important) and chemotactic factors from the mast cells in the nasal mucosa. There is a subsequent increase in epithelial permeability and this prompts migration of inflammatory cells to the area: […] Acute-phase response (minutes): Sneezing occurs within minutes of exposure, due to stimulation of afferent nerve endings. Increase in nasal secretion follows shortly afterwards, to peak 15-20 minutes after contact with the allergen. […] Late-phase response (6-12 hours): Characterised by nasal obstruction (although some of the acute symptoms may persist).
  • #15 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/134825-overview
    The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction. […] Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days. […] Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
  • #16 Types of Allergies – Global Allergy & Airways Patient PlatformExpandExpandExpandExpandExpandExpandToggle MenuScroll to topScroll to topExpandExpandExpandExpandExpandExpand
    https://gaapp.org/diseases/allergies/types-of-allergies
    During the early phase reaction chemical mediators released by mast cells including histamine, prostaglandins, leukotrienes and thromboxane produce local tissue responses characteristic of an allergic reaction. […] These observations suggest that IgE is instrumental in the immune system’s response to allergens by virtue of its ability to trigger mast cell mediator release, leading directly to both the early and late phase reactions.
  • #17 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    A variety of mediators are released by these cells including leukotrienes, kinins, histamine which result in the continuation of the symptoms and the development of the late phase. […] The key to the orchestration of the late phase response lies in the production and release of a variety of cytokines and chemokines like IL-4, IL-13 from mast cells as these cytokines can upregulate the expression of 'adhesion molecules’ like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. […] Mast cells play a central role in the immune mechanisms of allergic rhinitis. […] In patients with allergic rhinitis mast cells are found to abundantly accumulate in the epithelial compartment of the nasal mucosa and these are predominantly of the MC (T) phenotype.
  • #18 Allergic Rhinitis: Practice Essentials, Background, Pathophysiology
    https://emedicine.medscape.com/article/134825-overview
    The mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin. The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2. These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions. Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction. […] Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages. This results in continued inflammation, termed the late-phase response. The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur. The late phase may persist for hours or days. […] Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory response. These symptoms often contribute to impaired quality of life.
  • #19 Treatments for Seasonal Allergic Rhinitis | Effective Health Care (EHC) Program
    https://effectivehealthcare.ahrq.gov/products/allergy-seasonal/research-protocol
    Ongoing, prolonged allergen exposure and repeated late-phase responses lead to progressive inflammation of the nasal mucosa and increased allergen sensitivity. The amount of allergen capable of eliciting an allergic response lessens over time, an effect termed priming. The priming effect is thought to explain the development of mucosal hyper-responsiveness to nonallergen triggers, such as strong odors, cigarette smoke, and cold temperatures. […] It also provides the rationale for initiating effective rhinitis therapies prophylactically before the commencement of pollen season.
  • #20 Overview: Hay fever – InformedHealth.org – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK279488/
    Hay fever is an allergic reaction to pollen in the air, affecting the upper airways. The medical term for the symptoms it causes is allergic rhinitis. […] Allergy symptoms arise when your body overreacts to particular substances that are usually harmless, such as pollen. These substances (allergens) trigger a chain reaction in the immune system. First, antibodies to the allergen are made, and they bind to specific cells. If these cells come into contact with the allergen again, they are then able to respond by releasing chemical substances such as histamine. These substances then lead to allergic reactions such as sneezing or itchy eyes. […] Severe hay fever may increase the likelihood of developing other medical conditions such as sinusitis (inflammation of the sinuses). Hay fever often makes the mucous membranes lining the airways overly sensitive in general too. As a result, they may also react more strongly to irritants like dry air in heated rooms or cigarette smoke.
  • #21 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    The production of IgE locally in the nasal mucosa is now well established. […] The locally produced IgE then can play a key role in mast cell activity amplification via upregulating the FcRI expression in mast cells and subsequent mediator release after crosslinking of the bound IgE. […] Nerve growth factor (NGF) which is over expressed in allergic rhinitis is linked to the development of hyperresponsiveness, and is also associated with allergic inflammation, thus bridging the gap between these two features of allergic rhinitis and asthma. […] There is evidence of ongoing inflammation in the airway even when rhinitis or asthma symptoms are quiescent. […] AR is not associated with just localized inflammation of the nasal mucosa but also has a systemic element to it. […] The increasing evidence on the links between AR and asthma comes from epidemiologic, immunologic, and clinical studies.
  • #22 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    A variety of mediators are released by these cells including leukotrienes, kinins, histamine which result in the continuation of the symptoms and the development of the late phase. […] The key to the orchestration of the late phase response lies in the production and release of a variety of cytokines and chemokines like IL-4, IL-13 from mast cells as these cytokines can upregulate the expression of 'adhesion molecules’ like vascular cell adhesion molecule 1 (VCAM-1) on the endothelial cells facilitating the infiltration of eosinophils, T lymphocytes and basophils into the nasal mucosa. […] Mast cells play a central role in the immune mechanisms of allergic rhinitis. […] In patients with allergic rhinitis mast cells are found to abundantly accumulate in the epithelial compartment of the nasal mucosa and these are predominantly of the MC (T) phenotype.
  • #23 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Mast cells also induce IgE synthesis in B cells and as will be described later in this article, mast cells play a key role via the IgE-IgE receptor mast cell cascade. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. […] Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] Within the tissue, cytokines like IL-5 and GM-SCF keep eosinophils alive for several days or even weeks which overcome programmed cell death (apoptosis). […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. […] The ligand for the chemokine TARC, CCR4, was found to be expressed by Th2 cells. […] Mucosal inflammation in allergic rhinitis is characterized by the tissue infiltration of T lymphocytes (CD4+ T cells, and CD25+ (activated) T cells) both in the submucosa and the epithelium.
  • #24 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    The production of IgE locally in the nasal mucosa is now well established. […] The locally produced IgE then can play a key role in mast cell activity amplification via upregulating the FcRI expression in mast cells and subsequent mediator release after crosslinking of the bound IgE. […] Nerve growth factor (NGF) which is over expressed in allergic rhinitis is linked to the development of hyperresponsiveness, and is also associated with allergic inflammation, thus bridging the gap between these two features of allergic rhinitis and asthma. […] There is evidence of ongoing inflammation in the airway even when rhinitis or asthma symptoms are quiescent. […] AR is not associated with just localized inflammation of the nasal mucosa but also has a systemic element to it. […] The increasing evidence on the links between AR and asthma comes from epidemiologic, immunologic, and clinical studies.
  • #25 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Mast cells also induce IgE synthesis in B cells and as will be described later in this article, mast cells play a key role via the IgE-IgE receptor mast cell cascade. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. […] Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] Within the tissue, cytokines like IL-5 and GM-SCF keep eosinophils alive for several days or even weeks which overcome programmed cell death (apoptosis). […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. […] The ligand for the chemokine TARC, CCR4, was found to be expressed by Th2 cells. […] Mucosal inflammation in allergic rhinitis is characterized by the tissue infiltration of T lymphocytes (CD4+ T cells, and CD25+ (activated) T cells) both in the submucosa and the epithelium.
  • #26 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Mast cells also induce IgE synthesis in B cells and as will be described later in this article, mast cells play a key role via the IgE-IgE receptor mast cell cascade. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. […] Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] Within the tissue, cytokines like IL-5 and GM-SCF keep eosinophils alive for several days or even weeks which overcome programmed cell death (apoptosis). […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. […] The ligand for the chemokine TARC, CCR4, was found to be expressed by Th2 cells. […] Mucosal inflammation in allergic rhinitis is characterized by the tissue infiltration of T lymphocytes (CD4+ T cells, and CD25+ (activated) T cells) both in the submucosa and the epithelium.
  • #27 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    There is a significant correlation between the increase in CD4+ T cells during the late phase allergic reaction following an allergen challenge and the number of infiltrating eosinophils in the mucosa. […] Allergic reactions occur in a mucosal environment that is rich in both dendritic cells and macrophages. […] However, there are significant differences between the lower and upper airways, as alveolar macrophages form more than 90% of the cell population in bronchial alveolar lavage, but airway macrophages on the nasal epithelial surface just account for about 1 to 2% of the cells. […] It is now appreciated that allergens, on account of their enzymatic proteolytic activity can directly activate cells. […] Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation.
  • #28 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Mast cells also induce IgE synthesis in B cells and as will be described later in this article, mast cells play a key role via the IgE-IgE receptor mast cell cascade. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. […] Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] Within the tissue, cytokines like IL-5 and GM-SCF keep eosinophils alive for several days or even weeks which overcome programmed cell death (apoptosis). […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. […] The ligand for the chemokine TARC, CCR4, was found to be expressed by Th2 cells. […] Mucosal inflammation in allergic rhinitis is characterized by the tissue infiltration of T lymphocytes (CD4+ T cells, and CD25+ (activated) T cells) both in the submucosa and the epithelium.
  • #29 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Mast cells also induce IgE synthesis in B cells and as will be described later in this article, mast cells play a key role via the IgE-IgE receptor mast cell cascade. […] Eosinophils play an important role in chronic allergic diseases, making them major targets for basic and therapeutic research. […] Eotaxin appears to be critical for the maturation and release of eosinophils from the bone marrow. […] Within the tissue, cytokines like IL-5 and GM-SCF keep eosinophils alive for several days or even weeks which overcome programmed cell death (apoptosis). […] T lymphocytes are among the principal factors that regulate and co-ordinate immune responses in allergic diseases. […] The ligand for the chemokine TARC, CCR4, was found to be expressed by Th2 cells. […] Mucosal inflammation in allergic rhinitis is characterized by the tissue infiltration of T lymphocytes (CD4+ T cells, and CD25+ (activated) T cells) both in the submucosa and the epithelium.
  • #30 Study Complicates Popular Theory Linking Allergies to Hygiene and Microbes | American Association for the Advancement of Science (AAAS)
    https://www.aaas.org/news/study-complicates-popular-theory-linking-allergies-hygiene-and-microbes
    The reason for this increase in allergic diseases in the modern world is still not very clear. […] Although there is increasing evidence how microbiota regulates different immune responses, … there is no known mechanism for how diversity of microbial environment influences the development and management of allergies. […] Essentially, they took genetically standardized, pathogen-free baby mice and placed them in semi-natural environments with hay, compost and contaminated particles called fomites from truly wild mice. […] Importantly, it does so from the moment the mice are born, which was critical, since microbial exposures as newborns and infants are thought to play the greatest role in protecting us from allergy. […] When we talk about a type 2 immune response, we are talking about cells that produce specific cytokines that directly trigger the symptoms of allergic diseases and asthma.
  • #31 Study Complicates Popular Theory Linking Allergies to Hygiene and Microbes | American Association for the Advancement of Science (AAAS)
    https://www.aaas.org/news/study-complicates-popular-theory-linking-allergies-hygiene-and-microbes
    In particular, the wildings were marked by expansion of newly differentiated type 2 helper T (TH2) cell and existing memory TH2 cells in the lungs. Those cells can produce chemicals that signal to eosinophils and can help trigger asthma and airway inflammation. […] Our study shows that manipulation of the microbiota to improve health is not straightforward and that we need to consider not only when in life infections are acquired, but also the sequence and duration of microbial exposures. […] Ultimately, according to Rosshart, the study’s main takeaway revolves around the concept of health as a multi-faceted state with compounding factors or „little things,” which include genetics, microbial exposures and environmental conditions.
  • #32 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    There is a significant correlation between the increase in CD4+ T cells during the late phase allergic reaction following an allergen challenge and the number of infiltrating eosinophils in the mucosa. […] Allergic reactions occur in a mucosal environment that is rich in both dendritic cells and macrophages. […] However, there are significant differences between the lower and upper airways, as alveolar macrophages form more than 90% of the cell population in bronchial alveolar lavage, but airway macrophages on the nasal epithelial surface just account for about 1 to 2% of the cells. […] It is now appreciated that allergens, on account of their enzymatic proteolytic activity can directly activate cells. […] Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation.
  • #33 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    There is a significant correlation between the increase in CD4+ T cells during the late phase allergic reaction following an allergen challenge and the number of infiltrating eosinophils in the mucosa. […] Allergic reactions occur in a mucosal environment that is rich in both dendritic cells and macrophages. […] However, there are significant differences between the lower and upper airways, as alveolar macrophages form more than 90% of the cell population in bronchial alveolar lavage, but airway macrophages on the nasal epithelial surface just account for about 1 to 2% of the cells. […] It is now appreciated that allergens, on account of their enzymatic proteolytic activity can directly activate cells. […] Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation.
  • #34 Allergic rhinitis – Wikipedia
    https://en.wikipedia.org/wiki/Allergic_rhinitis
    Disruption of the nasal mucosal epithelial barrier may also release alarmins (a type of damage associated molecular pattern (DAMP) molecule) such as thymic stromal lymphopoietin, IL-25 and IL-33 which activate group 2 innate lymphoid cells (ILC2) which then also releases inflammatory cytokines leading to activation of immune cells.
  • #35 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    There is a significant correlation between the increase in CD4+ T cells during the late phase allergic reaction following an allergen challenge and the number of infiltrating eosinophils in the mucosa. […] Allergic reactions occur in a mucosal environment that is rich in both dendritic cells and macrophages. […] However, there are significant differences between the lower and upper airways, as alveolar macrophages form more than 90% of the cell population in bronchial alveolar lavage, but airway macrophages on the nasal epithelial surface just account for about 1 to 2% of the cells. […] It is now appreciated that allergens, on account of their enzymatic proteolytic activity can directly activate cells. […] Epithelial cell-derived thymic stromal lymphopoietin (TSLP) is a master switch for asthma or atopic dermatitis by inducing a dendritic cell-mediated Th2-type allergic inflammation.
  • #36 Azthena logo with the word Azthena
    https://www.news-medical.net/health/Allergies-and-Genetics.aspx
    Specific gene variations that alter the encoding of epithelial cell-derived cytokines such as interleukin-33 and thymic stromal lymphopoietin may be involved in the pathogenesis of allergies. […] It is likely that each of these factors may play in the pathogenesis of allergies, particularly for individuals who have a genetic susceptibility to the condition.
  • #37 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    The production of IgE locally in the nasal mucosa is now well established. […] The locally produced IgE then can play a key role in mast cell activity amplification via upregulating the FcRI expression in mast cells and subsequent mediator release after crosslinking of the bound IgE. […] Nerve growth factor (NGF) which is over expressed in allergic rhinitis is linked to the development of hyperresponsiveness, and is also associated with allergic inflammation, thus bridging the gap between these two features of allergic rhinitis and asthma. […] There is evidence of ongoing inflammation in the airway even when rhinitis or asthma symptoms are quiescent. […] AR is not associated with just localized inflammation of the nasal mucosa but also has a systemic element to it. […] The increasing evidence on the links between AR and asthma comes from epidemiologic, immunologic, and clinical studies.
  • #38 Pathophysiology and Non-Pharmacological Management of Allergic Rhinitis
    https://clinmedjournals.org/articles/iaphcm/international-archives-of-public-health-and-community-medicine-iaphcm-4-050.php?jid=iaphcm
    Recent advances have suggested that additional pathways may contribute to the pathophysiology of allergic rhinitis including local synthesis of IgE in the nasal mucosa, the epithelial expression of cytokines that regulate Th2 cytokine responses (i.e., thymic stromal lymphopoietin, IL-25, and IL-33), and the activation of histamine receptors other than H1 and H2 such as H4-histamine receptors. […] The levels of tryptase and histamine were higher in the perennial allergic rhinitis than the seasonal allergic rhinitis. […] Mechanisms underlying the neuronal-based symptoms of allergy: Persons with allergies present with symptoms that often are the result of alterations in the nervous system. […] There is a definite relation between the symptoms of hyperparasympathetic nervous system and allergic rhinitis as one study results have indicated that patients with intermittent and mild AR have hypervagal activity and hyposympathetic activity, and the predominance lessens in patients with more persistent AR and severe symptoms.
  • #39 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    The production of IgE locally in the nasal mucosa is now well established. […] The locally produced IgE then can play a key role in mast cell activity amplification via upregulating the FcRI expression in mast cells and subsequent mediator release after crosslinking of the bound IgE. […] Nerve growth factor (NGF) which is over expressed in allergic rhinitis is linked to the development of hyperresponsiveness, and is also associated with allergic inflammation, thus bridging the gap between these two features of allergic rhinitis and asthma. […] There is evidence of ongoing inflammation in the airway even when rhinitis or asthma symptoms are quiescent. […] AR is not associated with just localized inflammation of the nasal mucosa but also has a systemic element to it. […] The increasing evidence on the links between AR and asthma comes from epidemiologic, immunologic, and clinical studies.
  • #40 Pathophysiology and Non-Pharmacological Management of Allergic Rhinitis
    https://clinmedjournals.org/articles/iaphcm/international-archives-of-public-health-and-community-medicine-iaphcm-4-050.php?jid=iaphcm
    Recent advances have suggested that additional pathways may contribute to the pathophysiology of allergic rhinitis including local synthesis of IgE in the nasal mucosa, the epithelial expression of cytokines that regulate Th2 cytokine responses (i.e., thymic stromal lymphopoietin, IL-25, and IL-33), and the activation of histamine receptors other than H1 and H2 such as H4-histamine receptors. […] The levels of tryptase and histamine were higher in the perennial allergic rhinitis than the seasonal allergic rhinitis. […] Mechanisms underlying the neuronal-based symptoms of allergy: Persons with allergies present with symptoms that often are the result of alterations in the nervous system. […] There is a definite relation between the symptoms of hyperparasympathetic nervous system and allergic rhinitis as one study results have indicated that patients with intermittent and mild AR have hypervagal activity and hyposympathetic activity, and the predominance lessens in patients with more persistent AR and severe symptoms.
  • #41 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    The production of IgE locally in the nasal mucosa is now well established. […] The locally produced IgE then can play a key role in mast cell activity amplification via upregulating the FcRI expression in mast cells and subsequent mediator release after crosslinking of the bound IgE. […] Nerve growth factor (NGF) which is over expressed in allergic rhinitis is linked to the development of hyperresponsiveness, and is also associated with allergic inflammation, thus bridging the gap between these two features of allergic rhinitis and asthma. […] There is evidence of ongoing inflammation in the airway even when rhinitis or asthma symptoms are quiescent. […] AR is not associated with just localized inflammation of the nasal mucosa but also has a systemic element to it. […] The increasing evidence on the links between AR and asthma comes from epidemiologic, immunologic, and clinical studies.
  • #42 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Both AR and asthma are inflammatory diseases and their inflammatory mechanisms are similar in that they are characterized by an inflammatory infiltrate made up of eosinophils, T cells, and mast cells that release several mediators, chemokines and cytokines, local and systemic IgE synthesis, and a systemic link via the bone marrow. […] Successful management of this chronic allergic respiratory syndrome requires an integrated view of the airways, understanding of their interactions, and an integrated approach of treatment also targeting systemic inflammation.
  • #43 Overview on the pathomechanisms of allergic rhinitis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC3206239/
    Both AR and asthma are inflammatory diseases and their inflammatory mechanisms are similar in that they are characterized by an inflammatory infiltrate made up of eosinophils, T cells, and mast cells that release several mediators, chemokines and cytokines, local and systemic IgE synthesis, and a systemic link via the bone marrow. […] Successful management of this chronic allergic respiratory syndrome requires an integrated view of the airways, understanding of their interactions, and an integrated approach of treatment also targeting systemic inflammation.
  • #44 Pathogenesis of allergic rhinitis (rhinosinusitis) – UpToDate
    https://www.uptodate.com/contents/pathogenesis-of-allergic-rhinitis-rhinosinusitis
    Pathogenesis of allergic rhinitis is presented in this topic review. […] Upon exposure to an allergen, atopic individuals respond by producing allergen-specific immunoglobulin E (sIgE). These IgE antibodies bind to IgE receptors on mast cells in the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the IgE antibodies are bridged on the cell surface by allergen, resulting in activation of the cell. Mast cells in the nasal tissues release preformed and granule-associated chemical mediators, which cause the symptoms of allergic rhinitis. […] Immunogenetics — The expression of allergic diseases of the upper airways reflects an autosomal dominant pattern of inheritance with incomplete penetrance. This inheritance pattern is manifested as a propensity to respond to inhalant allergen exposure by producing high levels of allergen-sIgE. The IgE response appears to be controlled by immune response genes located within the major histocompatibility complex (MHC) on chromosome 6.
  • #45
    https://link.springer.com/article/10.1007/s12016-025-09028-3
    When an allergen enters the body for the first time, antigen-presenting cells transmit it to Th cells, which become activated and secrete cytokines such as IL-4 and IL-13. […] Those cytokines act on sIgGB cells to reconstitute and produce sIgE at the mucosal level. […] Localized sIgE in the mucous membranes plays a key role in the local allergic inflammatory response, and a variety of cytokines and immune cells interact with each other to influence IgE synthesis and allergic processes. […] Genomic studies have found a genetic association regarding AR pathogenesis. […] According to estimates, AR has a high hereditary component, with a heritability index of 0.65. […] Several reports have linked genetic loci and candidate genes to AR. […] Various causative genes of AR (e.g., SDAD1, CXCL10, and CXCL9) have been found to be related to an array of immune-related disorders.
  • #46
    https://link.springer.com/article/10.1007/s12016-025-09028-3
    Those genes affect common genetic risk variants for atopic diseases, which implies that they can display typical pathogenic traits and be used for creating novel treatments. […] Epigenetic studies of AR have focused on several core aspects covering the regulation of gene expression, DNA methylation, histone modifications, and the role of non-coding RNAs. […] Research has demonstrated a correlation between the quantity and pattern of CD4+T cells in AR and the DNA methylation pattern, which can be used to differentiate allergic patients from healthy individuals. […] DNA methylation is involved in the progression and therapeutic efficacy of AR in multiple ways. […] Metabolomics focuses on the discovery of new biomarkers and the monitoring of therapeutic effects. […] Specific metabolomic profiling of samples, including induced sputum, respiratory condensate, bronchoalveolar lavage fluid, serum, plasma, and lung tissues, reflect the different phenotypes, inflammatory patterns, and eventual outcomes of a disease.
  • #47
    https://link.springer.com/article/10.1007/s12016-025-09028-3
    Those genes affect common genetic risk variants for atopic diseases, which implies that they can display typical pathogenic traits and be used for creating novel treatments. […] Epigenetic studies of AR have focused on several core aspects covering the regulation of gene expression, DNA methylation, histone modifications, and the role of non-coding RNAs. […] Research has demonstrated a correlation between the quantity and pattern of CD4+T cells in AR and the DNA methylation pattern, which can be used to differentiate allergic patients from healthy individuals. […] DNA methylation is involved in the progression and therapeutic efficacy of AR in multiple ways. […] Metabolomics focuses on the discovery of new biomarkers and the monitoring of therapeutic effects. […] Specific metabolomic profiling of samples, including induced sputum, respiratory condensate, bronchoalveolar lavage fluid, serum, plasma, and lung tissues, reflect the different phenotypes, inflammatory patterns, and eventual outcomes of a disease.
  • #48
    https://link.springer.com/article/10.1007/s12016-025-09028-3
    Those genes affect common genetic risk variants for atopic diseases, which implies that they can display typical pathogenic traits and be used for creating novel treatments. […] Epigenetic studies of AR have focused on several core aspects covering the regulation of gene expression, DNA methylation, histone modifications, and the role of non-coding RNAs. […] Research has demonstrated a correlation between the quantity and pattern of CD4+T cells in AR and the DNA methylation pattern, which can be used to differentiate allergic patients from healthy individuals. […] DNA methylation is involved in the progression and therapeutic efficacy of AR in multiple ways. […] Metabolomics focuses on the discovery of new biomarkers and the monitoring of therapeutic effects. […] Specific metabolomic profiling of samples, including induced sputum, respiratory condensate, bronchoalveolar lavage fluid, serum, plasma, and lung tissues, reflect the different phenotypes, inflammatory patterns, and eventual outcomes of a disease.
  • #49
    https://link.springer.com/article/10.1007/s12016-025-09028-3
    The production of key inflammatory mediators by the arachidonic acid (AA) metabolic network is considered to be a hallmark of various inflammation-related diseases. […] The microbiome, often referred to as the second human genome, refers to the composition, function, and interactions of the host microbial community, which is a major component of the immune system. […] Increasing evidence suggests that patients with allergic diseases such as asthma, food allergy, atopic dermatitis, and AR have dysbiosis of the gut microbiota. […] Combined multi-omic studies of AR from different perspectives can provide a more thorough and organized grasp of the pathophysiological mechanisms and individual differences of AR. […] Such studies can comprehensively analyze the genomic, transcriptomic, proteomic, and metabolomic multi-omics data of patients and facilitate the design of precise treatment regimens.
  • #50 Combattre les allergies – L’actu de l’Institut Pasteur
    https://www.pasteur.fr/en/home/research-journal/reports/tackling-allergies
    IgE antibodies are generally blamed for allergic reactions, but we have demonstrated in experimental models that during anaphylaxis, another antibody family, IgG antibodies, may be the main cause of the reaction. […] Apart from the specific case of anaphylactic shock, standard first-line allergy treatments are designed to address the symptoms. […] The idea is to teach the body to tolerate the allergen by giving the patient small doses of it (natural pollen extracts, mites, bee venom, etc.), via injection or sublingual delivery, over a period of several weeks or months and sometimes throughout their lifetime. […] We have shown how some bacteria in the microbiota specifically block the immune responses involved in allergic reactions. […] An imbalance in the diversity of an individual’s microbiota could encourage allergic responses.
  • #51 Yes, Climate Change Really is Making Your Hay Fever Worse | TIME
    https://time.com/7276018/how-climate-change-is-making-hay-fever-worse/
    As climate change worsens, so too do allergy symptoms. […] Increasingly, health care professionals are concluding that as global heat increases so too do allergy symptoms. […] The study is whats known as a scoping review of the literature, one that takes the measure of the body of papers published on a particular topic in a particular time frame and seeks to come away with an idea of what the emerging consensus is on the science. […] A little over half of the studies Pershad and her colleagues looked at reported longer pollen seasons or higher pollen concentrationsor bothlinked to climate change. […] Individual studies deepened the link between climate and hay fever. […] The papers in the survey also looked at the mechanism that links climate change to increases in hay fever. […] A pair of studies both in the wild and in the lab showed that greater humidity and higher levels of carbon dioxidewhich is a known growth and reproductive stimulator of plantsincrease the dispersal of allergenic pollen. […] Global warming is exacerbating weather extremes such as hurricanes and flooding, which increase the risk of mold growth, a common environmental allergen.
  • #52 Yes, Climate Change Really is Making Your Hay Fever Worse | TIME
    https://time.com/7276018/how-climate-change-is-making-hay-fever-worse/
    As climate change worsens, so too do allergy symptoms. […] Increasingly, health care professionals are concluding that as global heat increases so too do allergy symptoms. […] The study is whats known as a scoping review of the literature, one that takes the measure of the body of papers published on a particular topic in a particular time frame and seeks to come away with an idea of what the emerging consensus is on the science. […] A little over half of the studies Pershad and her colleagues looked at reported longer pollen seasons or higher pollen concentrationsor bothlinked to climate change. […] Individual studies deepened the link between climate and hay fever. […] The papers in the survey also looked at the mechanism that links climate change to increases in hay fever. […] A pair of studies both in the wild and in the lab showed that greater humidity and higher levels of carbon dioxidewhich is a known growth and reproductive stimulator of plantsincrease the dispersal of allergenic pollen. […] Global warming is exacerbating weather extremes such as hurricanes and flooding, which increase the risk of mold growth, a common environmental allergen.
  • #53 Hay Fever Allergy: A Comprehensive Guide – Wellness People
    https://thewellnesspeople.co/managing-hay-fever-allergy/
    When ones body is exposed to pollen, it triggers an auto-immune response from the body, causing the release of antibodies called immunoglobulin E (IgE), which, in turn, releases a substance called histamine in the body. It is histamine that causes the typical symptoms of Hay Fever. […] Instances of hay fever are on the rise due to climate change, as warmer and windier weather helps pollen travel farther and remain in the air longer. Increasing air pollution is also a leading cause. […] Since the antibodies generated in response to pollen entering our bodies lead to the release of histamine, antihistamines are prescribed to deal with the symptoms of hay fever.
  • #54 Seasonal Hay Fever Warning Signs & What To Do | OneWelbeck
    https://onewelbeck.com/news/treatments-for-seasonal-hayfever/
    Hay fever, or allergic rhinitis, is a common condition that affects between 10-15% of children and 26% of adults in the UK. […] If you’ve got hay fever, which is affecting your quality of life, it’s important to see an experienced allergist, Dr Rutkowski explained. […] immunotherapy which addresses the mechanism of your condition and helps reduce hay fever symptoms in the long-term. […] It occurs when your immune system overreacts to allergens like grass and tree pollen, house dust mites or animal dander, making your eyes and nasal passages itchy and inflamed. […] Allergy means that unfortunately, our immune system decides to fight with the environment. […] Hay fever and allergic asthma are often much worse, for example, in kids growing up in inner cities or built-up areas with lots of motorways because of the pollution.
  • #55 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    An allergy is an unnecessary immune response to an innocuous substance (an allergen). […] Allergic reactions can be grouped into two classes. The most common and best understood is mediated by a class of antibody called immunoglobulin E (IgE). […] The type of symptoms depends mainly on how the person is exposed to the allergen. […] The ‘Hygiene Hypothesis’, the idea that increased exposure to microorganisms correlates with a decreased tendency to develop allergy, is one explanation for the rise in prevalence. […] Allergy immunotherapy or desensitisation can be used in some cases to eliminate a person’s allergy by reversing their immune response to the triggering allergen. […] The process through which a person’s body becomes sensitive to a given allergen is known as sensitisation.
  • #56 Study Complicates Popular Theory Linking Allergies to Hygiene and Microbes | American Association for the Advancement of Science (AAAS)
    https://www.aaas.org/news/study-complicates-popular-theory-linking-allergies-hygiene-and-microbes
    New and unexpected findings in mice challenge a widespread theory that connects a perceived rise in allergies and asthma to the emergence of modern hygiene. This idea, called the hygiene hypothesis, suggests that allergies come from overreactive and bored immune systems without enough exposures to bacteria, fungi and parasites. […] After raising laboratory mice in semi-natural settings with ample microbes, Rosshart and his colleagues found that the „wilding” mice still responded strongly to allergen challenge tests. These surprising results show that the relationship between microbiota and the immune system is more complicated than understood. […] The hygiene hypothesis dictates that as the world became more sanitation-focused, people encountered fewer germs and parasites. This lack of stimulation for the immune system led white blood cells — especially eosinophils, which defend against parasitic infections that are no longer as commonplace — to behave in dysfunctional ways.
  • #57 Study Complicates Popular Theory Linking Allergies to Hygiene and Microbes | American Association for the Advancement of Science (AAAS)
    https://www.aaas.org/news/study-complicates-popular-theory-linking-allergies-hygiene-and-microbes
    New and unexpected findings in mice challenge a widespread theory that connects a perceived rise in allergies and asthma to the emergence of modern hygiene. This idea, called the hygiene hypothesis, suggests that allergies come from overreactive and bored immune systems without enough exposures to bacteria, fungi and parasites. […] After raising laboratory mice in semi-natural settings with ample microbes, Rosshart and his colleagues found that the „wilding” mice still responded strongly to allergen challenge tests. These surprising results show that the relationship between microbiota and the immune system is more complicated than understood. […] The hygiene hypothesis dictates that as the world became more sanitation-focused, people encountered fewer germs and parasites. This lack of stimulation for the immune system led white blood cells — especially eosinophils, which defend against parasitic infections that are no longer as commonplace — to behave in dysfunctional ways.
  • #58 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text
    https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1
    The pathophysiology of AR is complex, comprising an early- and late-phase allergic response. […] The early-phase reaction is characterised by mast cell degranulation. […] The late-phase reaction develops over a period of hours after exposure to an allergen. […] This late-phase inflammatory reaction is associated with tissue remodelling, further tissue oedema, and the development and perpetuation of nasal congestion, considered by patients to be one of the most troublesome symptoms of AR. […] As a result of mucosal inflammation, tissues become primed and react more vigorously to allergen exposure. […] The pharmacological profiles of available treatments for AR show that there are a number of pathophysiological gaps within the AR pharmacopeia. […] No single medication class is capable of providing rapid and complete relief from all symptoms associated with AR.
  • #59 The complex pathophysiology of allergic rhinitis: scientific rationale for the development of an alternative treatment option | Allergy, Asthma & Clinical Immunology | Full Text
    https://aacijournal.biomedcentral.com/articles/10.1186/s13223-018-0314-1
    MP-AzeFlu comprises an INAH (AZE), an INS (FP), and a novel formulation in a single spray. […] It therefore offers the benefits of broad pathophysiological coverage due to incorporation of two agents from different medication classes with different yet complementary modes of action, antagonises both early- and late-phase allergic responses, and is convenient to use. […] MP-AzeFlu blocks two important pathophysiological pathways involved in the early- and late-phase reactions in the disease, providing rapid relief from all symptoms associated with AR.
  • #60 Overview: Hay fever – InformedHealth.org – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK279488/
    Allergen-specific immunotherapy (also known as desensitization) can reduce your sensitivity to allergens over the long term. Like with vaccines, this treatment approach involves exposing people to small amounts of the allergen. Here it is done at regular intervals by either injecting the allergen under your skin or placing it under your tongue. Allergen-specific immunotherapy takes at least three to five years to complete.
  • #61 Treatment of Allergic Rhinitis | AAFP
    https://www.aafp.org/pubs/afp/issues/2015/1201/p985.html
    Histamine is the most studied mediator in early allergic response. It causes smooth muscle constriction, mucus secretion, vascular permeability, and sensory nerve stimulation, resulting in the symptoms of allergic rhinitis. […] The leukotriene D4 receptor antagonist montelukast (Singulair) is comparable to oral antihistamines but is less effective than intranasal corticosteroids.2,16,36 It may be particularly useful in patients with coexistent asthma because it reduces bronchospasm and attenuates the inflammatory response.2 […] Immunotherapy should be considered for moderate or severe persistent allergic rhinitis that is not responsive to usual treatments, in patients who cannot tolerate standard therapies or who want to avoid long-term medication use, and in patients with allergic asthma.2,3,13,16,17,31,4346 Targeted immunotherapy, the only treatment that changes the natural course of allergic rhinitis, consists of administering a small amount of allergen extract subcutaneously or sublingually.44
  • #62 Allergy | British Society for Immunology
    https://www.immunology.org/policy-and-public-affairs/briefings-and-position-statements/allergy
    Allergy research has established a way to reverse a person’s allergy development in some cases. […] During AIT, the immune system’s responses change. These changes may include producing less IgE, producing ‘blocking’ IgG antibodies, and producing more regulatory T cells, promoting tolerance and a less active immune response. […] However, the exact mechanism behind desensitisation is not yet known and it is likely that different patients exhibit different immune profiles following the treatment.
  • #63 Seasonal Hay Fever Warning Signs & What To Do | OneWelbeck
    https://onewelbeck.com/news/treatments-for-seasonal-hayfever/
    However it is crucial to be allergy tested to identify the exact allergen(s) that triggers your hay fever and help you manage them more effectively. […] We can suppress and control symptoms by changing how your immune system interacts with pollen/house dust mites/pet allergens. This is called immunotherapy or desensitisation. […] Immunotherapy, or desensitisation therapy, is a ground-breaking allergy treatment that can reduce your body’s response to allergens and ease hay fever symptoms. […] In immunotherapy, we give you increasing doses of the relevant pollen extract depending on your diagnosis (tree or grass pollen etc). […] We can address the origin of the problem and train your body to stop reacting to allergens, without interfering with other parts of your immune system. […] Although not a cure, immunotherapy modifies the disease process so that many patients can feel like they no longer have hay fever.
  • #64 How to Tape for Hay Fever (Allergic Rhinitis) with CureTape
    https://www.thysol.co.uk/how-to-tape/hay-fever-allergic-rhinitis/
    Kinesiology taping for hay fever is based on the principle that external skin stimulation can have a reflective influence on the tissue structures of the spinal cord segments belonging to the innervation area. […] Hay fever is an allergic reaction to the pollen of shrubs, grasses and trees. In hay fever sufferers, the immune system reacts as soon as pollen enters the body. The body then produces the antibody IgE (Immunoglobin E). The IgE binds to mast cells and basophilic granulocytes. […] Histamine is released and causes the allergic reactions typical of hay fever. The blood vessels dilate and start leaking. It also causes the smooth muscle cells in the lungs to contract. […] The treatment with tape consists of segmental support by a dorsal back tape applied to this lung area. A possible explanation of reduced complaints can be found in the calming effect of the allergic reaction mechanism. The sympathetic system comes to rest.
  • #65 How to Tape for Hay Fever (Allergic Rhinitis) with CureTape
    https://www.thysol.co.uk/how-to-tape/hay-fever-allergic-rhinitis/
    The fascia contains many sensors. By applying the tape to the skin, you provide a sensory stimulus to the fascia, which creates a different tension; the connective tissue comes to rest. This, in turn, has a positive impact on the immune system, reducing the body’s response to hay fever and creating substances for an allergic reaction. […] Presumably the tension of the fascia and/or the stimulation of the sensors in the skin has a positive effect on the influence of the immunoglobulin IgE and therefore indirectly on the release of histamine. […] In both the 2016 and 2017 inventories, 84% of hay fever patients indicated that their symptoms decreased after applying the hay fever tape as part of the Kinesiology taping Concept. […] In 84% of the participants, there was a reduction in symptoms after one, two and/or three taping sessions. For some symptoms, the reduction in symptoms was spectacular, with a VAS score of up to 80%. […] The combi-tape (back and chest) gave the best result.
  • #66 Hay Fever 101: Living with Seasonal Allergies | LewisGale Physicians
    https://lgphysicians.com/about/newsroom/hay-fever-101-living-with-seasonal-allergies
    Conventional treatment for hay fever involves non-sedating antihistamines and nasal steroids that are usually quite effective. In addition, some people treat their allergy symptoms with allergy shots. Known as immunotherapy, the idea behind the treatment is to reduce allergic symptoms and increase immunity against the allergic substance by exposing the body to small amounts of the substance. Traditionally, exposure is done through injecting the allergic substance into the upper arm. This is extremely effective for treating allergic rhinitis and has minimal adverse effects when done under the supervision of an allergist. […] Some homeopathic treatments show promise, with several small studies having positive results using medicinal herbs to treat allergy symptoms. One study looked at a combination tablet containing Cinnamomum zeylanicum, Malpighia glabra, and Bidens pilosa versus the well-known antihistamine, loratadine. The researchers found that both loratadine and the combination herbal tablet reduced nasal symptoms.
  • #67 Hay Fever 101: Living with Seasonal Allergies | LewisGale Physicians
    https://lgphysicians.com/about/newsroom/hay-fever-101-living-with-seasonal-allergies
    Another study compared the herb butterbur against fexofenadine (an over-the-counter allergy medication) and placebo. Butterbur and fexofenadine were found to be equally effective, while both were more effective than the placebo. Other promising natural remedies include acupuncture and sub-lingual immunotherapy (SLIT), an alternative to shots, where the allergic substance is placed under the tongue.
  • #68 Allergic Cascade: Mechanism of Reaction & Early vs. Late Phase
    https://www.medicinenet.com/allergic_cascade/article.htm
    The allergic cascade refers to allergic reactions that happen in the body in response to allergens. A variety of immune cells and chemical messengers participate in the allergic cascade. Symptoms of the allergic cascade range from mild swelling and itching to full-blown anaphylactic shock. […] The end result is a well-defined constellation of signs and symptoms produced by the „allergic cascade.” […] The balance between allergy-promoting TH2 cells and infection-fighting TH1 cells has been found to be a critical component of our immune system. […] The eosinophils appear to be particularly troublesome cells of inflammation. Eosinophils evolved to defend the body against parasites, much like IgE. […] The late-phase reaction involves an influx of a variety of inflammatory cells (eosinophils, neutrophils, lymphocytes, and mast cells) to the affected area, and if repeated inhalations of allergens cause recurrent reactions, these reactions may merge into each other leading to chronic or persistent allergic asthma. […] The most important of these chemical mediators is histamine. […] Current research is aimed at finding medications that target specific steps in the allergic cascade.