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NOD1-Mediated Mucosal Host Defense against Helicobacter pylori

Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th...

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Detalles Bibliográficos
Autores principales: Watanabe, Tomohiro, Asano, Naoki, Kitani, Atsushi, Fuss, Ivan J., Chiba, Tsutomu, Strober, Warren
Formato: Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989736/
https://www.ncbi.nlm.nih.gov/pubmed/21152124
http://dx.doi.org/10.4061/2010/476482
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author Watanabe, Tomohiro
Asano, Naoki
Kitani, Atsushi
Fuss, Ivan J.
Chiba, Tsutomu
Strober, Warren
author_facet Watanabe, Tomohiro
Asano, Naoki
Kitani, Atsushi
Fuss, Ivan J.
Chiba, Tsutomu
Strober, Warren
author_sort Watanabe, Tomohiro
collection PubMed
description Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1) in gastric epithelial cells plays an important role in innate immune responses against H. pylori. The detection of H. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense against H. pylori infection of the stomach.
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spelling pubmed-29897362010-12-09 NOD1-Mediated Mucosal Host Defense against Helicobacter pylori Watanabe, Tomohiro Asano, Naoki Kitani, Atsushi Fuss, Ivan J. Chiba, Tsutomu Strober, Warren Int J Inflam Review Article Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1) in gastric epithelial cells plays an important role in innate immune responses against H. pylori. The detection of H. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense against H. pylori infection of the stomach. SAGE-Hindawi Access to Research 2010-07-15 /pmc/articles/PMC2989736/ /pubmed/21152124 http://dx.doi.org/10.4061/2010/476482 Text en Copyright © 2010 Tomohiro Watanabe et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Watanabe, Tomohiro
Asano, Naoki
Kitani, Atsushi
Fuss, Ivan J.
Chiba, Tsutomu
Strober, Warren
NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title_full NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title_fullStr NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title_full_unstemmed NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title_short NOD1-Mediated Mucosal Host Defense against Helicobacter pylori
title_sort nod1-mediated mucosal host defense against helicobacter pylori
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989736/
https://www.ncbi.nlm.nih.gov/pubmed/21152124
http://dx.doi.org/10.4061/2010/476482
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