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Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa

Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gas...

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Autores principales: Nedrud, John G., Czinn, Steven J., Ding, Hua, Zagorski, Brandon M., Redline, Raymond W., Twaddell, William, Blanchard, Thomas G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389333/
https://www.ncbi.nlm.nih.gov/pubmed/22783255
http://dx.doi.org/10.3389/fimmu.2012.00181
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author Nedrud, John G.
Czinn, Steven J.
Ding, Hua
Zagorski, Brandon M.
Redline, Raymond W.
Twaddell, William
Blanchard, Thomas G.
author_facet Nedrud, John G.
Czinn, Steven J.
Ding, Hua
Zagorski, Brandon M.
Redline, Raymond W.
Twaddell, William
Blanchard, Thomas G.
author_sort Nedrud, John G.
collection PubMed
description Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gastritis, peptic ulcer disease, gastric MALT lymphoma, or gastric adenocarcinoma. The bacterial and host factors that determine clinical outcome and influence the development of widely varying diseases have not been elucidated. We compared disease in Helicobacter-infected severe combined immunodeficient (SCID) mice on different genetic backgrounds with their corresponding immunocompetent partners to determine if the genetics of the host significantly impacts the innate inflammatory outcome, independent of variations in bacterial virulence factors. BALB/c SCID and C57BL/6 SCID mice developed equivalent histologic gastritis by 8 weeks of infection. Immunocompetent BALB/c mice and C57BL/6 mice developed significantly lower or higher degrees of inflammation respectively. Innate inflammation in immunodeficient mice on the C57BL/6 background remained low even in the absence of the regulatory cytokine IL-10. These results demonstrate that adaptive immunity is not required for the generation of low level inflammation in response to Helicobacter infection and that the degree of inflammation is consistent among different genetic backgrounds. Additionally, this inflammation is limited even in the absence of regulatory T cells.
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spelling pubmed-33893332012-07-10 Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa Nedrud, John G. Czinn, Steven J. Ding, Hua Zagorski, Brandon M. Redline, Raymond W. Twaddell, William Blanchard, Thomas G. Front Immunol Immunology Helicobacter pylori (H. pylori) is a bacterial pathogen that resides at the gastric mucosa and has a world-wide prevalence of over 50%. Infection usually lasts for the life of the host, and although all infected individuals will develop histologic gastritis only a subset will develop symptomatic gastritis, peptic ulcer disease, gastric MALT lymphoma, or gastric adenocarcinoma. The bacterial and host factors that determine clinical outcome and influence the development of widely varying diseases have not been elucidated. We compared disease in Helicobacter-infected severe combined immunodeficient (SCID) mice on different genetic backgrounds with their corresponding immunocompetent partners to determine if the genetics of the host significantly impacts the innate inflammatory outcome, independent of variations in bacterial virulence factors. BALB/c SCID and C57BL/6 SCID mice developed equivalent histologic gastritis by 8 weeks of infection. Immunocompetent BALB/c mice and C57BL/6 mice developed significantly lower or higher degrees of inflammation respectively. Innate inflammation in immunodeficient mice on the C57BL/6 background remained low even in the absence of the regulatory cytokine IL-10. These results demonstrate that adaptive immunity is not required for the generation of low level inflammation in response to Helicobacter infection and that the degree of inflammation is consistent among different genetic backgrounds. Additionally, this inflammation is limited even in the absence of regulatory T cells. Frontiers Research Foundation 2012-07-04 /pmc/articles/PMC3389333/ /pubmed/22783255 http://dx.doi.org/10.3389/fimmu.2012.00181 Text en Copyright © 2012 Nedrud, Czinn, Ding, Zagorski, Redline, Twaddell and Blanchard. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
spellingShingle Immunology
Nedrud, John G.
Czinn, Steven J.
Ding, Hua
Zagorski, Brandon M.
Redline, Raymond W.
Twaddell, William
Blanchard, Thomas G.
Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title_full Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title_fullStr Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title_full_unstemmed Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title_short Lack of Genetic Influence on the Innate Inflammatory Response to Helicobacter Infection of the Gastric Mucosa
title_sort lack of genetic influence on the innate inflammatory response to helicobacter infection of the gastric mucosa
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389333/
https://www.ncbi.nlm.nih.gov/pubmed/22783255
http://dx.doi.org/10.3389/fimmu.2012.00181
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