The role of toll-like receptors in peptic ulcer disease

Helicobacter pylori (HP) is the primary etiologic factor that induces events in the immune system that lead to peptic ulcers. Toll-like receptors (TLRs) are an important part of the innate immune system, as they play pivotal roles in pathogen-associated molecular pattern (PAMP) recognition of HP as...

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Autores principales:	Shizhu Jin, Narayan Nepal, Yang Gao
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	toll-like receptor peptic ulcer disease helicobacter pylori pathogenesis virulence factors polymorphism Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/e1f32fee99dd4e6286721a2b98b7a033
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spelling	oai:doaj.org-article:e1f32fee99dd4e6286721a2b98b7a0332021-11-04T15:51:57ZThe role of toll-like receptors in peptic ulcer disease2578-582610.1080/25785826.2021.1963190https://doaj.org/article/e1f32fee99dd4e6286721a2b98b7a0332021-10-01T00:00:00Zhttp://dx.doi.org/10.1080/25785826.2021.1963190https://doaj.org/toc/2578-5826Helicobacter pylori (HP) is the primary etiologic factor that induces events in the immune system that lead to peptic ulcers. Toll-like receptors (TLRs) are an important part of the innate immune system, as they play pivotal roles in pathogen-associated molecular pattern (PAMP) recognition of HP as well host-associated damage-associated molecular patterns (DAMPs). Recent advancements such as COX-2 production, LPS recognition through TLR2, CagL, and CagY protein of HP activating TLR5, TLR9 activation via type IV secretion system (T4SS) using DNA transfer, TLR polymorphisms, their adaptor molecules, cytokines, and other factors play a significant role in PUD. Thus, some novel PUD treatments including Chuyou Yuyang granules, function by TLR4/NF‐κB signaling pathway suppression and TNF-α and IL-18 inhibition also rely on TLR signaling. Similarly glycyrrhetinic acid (GA) treatment activates TLR-4 in Ana-1 cells not via TRIF, but via MYD88 expression, which is significantly upregulated to cure PUD. Therefore, understanding TLR signaling complexity and its resultant immune modulation after host-pathogen interactions is pivotal to drug and vaccine development for other diseases as well including cancer and recent pandemic COVID-19. In this review, we summarize the TLRs and HP interaction; its pathophysiology-related signaling pathways, polymorphisms, and pharmaceutical approaches toward PUD.Shizhu JinNarayan NepalYang GaoTaylor & Francis Grouparticletoll-like receptorpeptic ulcer diseasehelicobacter pyloripathogenesisvirulence factorspolymorphismImmunologic diseases. AllergyRC581-607ENImmunological Medicine, Vol 0, Iss 0, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	toll-like receptor peptic ulcer disease helicobacter pylori pathogenesis virulence factors polymorphism Immunologic diseases. Allergy RC581-607
spellingShingle	toll-like receptor peptic ulcer disease helicobacter pylori pathogenesis virulence factors polymorphism Immunologic diseases. Allergy RC581-607 Shizhu Jin Narayan Nepal Yang Gao The role of toll-like receptors in peptic ulcer disease
description	Helicobacter pylori (HP) is the primary etiologic factor that induces events in the immune system that lead to peptic ulcers. Toll-like receptors (TLRs) are an important part of the innate immune system, as they play pivotal roles in pathogen-associated molecular pattern (PAMP) recognition of HP as well host-associated damage-associated molecular patterns (DAMPs). Recent advancements such as COX-2 production, LPS recognition through TLR2, CagL, and CagY protein of HP activating TLR5, TLR9 activation via type IV secretion system (T4SS) using DNA transfer, TLR polymorphisms, their adaptor molecules, cytokines, and other factors play a significant role in PUD. Thus, some novel PUD treatments including Chuyou Yuyang granules, function by TLR4/NF‐κB signaling pathway suppression and TNF-α and IL-18 inhibition also rely on TLR signaling. Similarly glycyrrhetinic acid (GA) treatment activates TLR-4 in Ana-1 cells not via TRIF, but via MYD88 expression, which is significantly upregulated to cure PUD. Therefore, understanding TLR signaling complexity and its resultant immune modulation after host-pathogen interactions is pivotal to drug and vaccine development for other diseases as well including cancer and recent pandemic COVID-19. In this review, we summarize the TLRs and HP interaction; its pathophysiology-related signaling pathways, polymorphisms, and pharmaceutical approaches toward PUD.
format	article
author	Shizhu Jin Narayan Nepal Yang Gao
author_facet	Shizhu Jin Narayan Nepal Yang Gao
author_sort	Shizhu Jin
title	The role of toll-like receptors in peptic ulcer disease
title_short	The role of toll-like receptors in peptic ulcer disease
title_full	The role of toll-like receptors in peptic ulcer disease
title_fullStr	The role of toll-like receptors in peptic ulcer disease
title_full_unstemmed	The role of toll-like receptors in peptic ulcer disease
title_sort	role of toll-like receptors in peptic ulcer disease
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/e1f32fee99dd4e6286721a2b98b7a033
work_keys_str_mv	AT shizhujin theroleoftolllikereceptorsinpepticulcerdisease AT narayannepal theroleoftolllikereceptorsinpepticulcerdisease AT yanggao theroleoftolllikereceptorsinpepticulcerdisease AT shizhujin roleoftolllikereceptorsinpepticulcerdisease AT narayannepal roleoftolllikereceptorsinpepticulcerdisease AT yanggao roleoftolllikereceptorsinpepticulcerdisease
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The role of toll-like receptors in peptic ulcer disease

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