Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.

Nucleotide oligomerisation domain 2 (NOD2) is a component of the innate immunity known to be involved in the homeostasis of Peyer patches (PPs) in mice. However, little is known about its role during gut infection in vivo. Yersinia pseudotuberculosis is an enteropathogen causing gastroenteritis, ade...

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Autores principales: Ulrich Meinzer, Sophie Esmiol-Welterlin, Frederick Barreau, Dominique Berrebi, Monique Dussaillant, Stephane Bonacorsi, Fabrice Chareyre, Michiko Niwa-Kawakita, Corinne Alberti, Ghislaine Sterkers, Claude Villard, Thecla Lesuffleur, Michel Peuchmaur, Michael Karin, Lars Eckmann, Marco Giovannini, Vincent Ollendorff, Hans Wolf-Watz, Jean-Pierre Hugot
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Publicado: Public Library of Science (PLoS) 2008
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spelling oai:doaj.org-article:1e13e916d8c84a198cf5492130e8020a2021-11-25T06:11:31ZNod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.1932-620310.1371/journal.pone.0002769https://doaj.org/article/1e13e916d8c84a198cf5492130e8020a2008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18648508/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Nucleotide oligomerisation domain 2 (NOD2) is a component of the innate immunity known to be involved in the homeostasis of Peyer patches (PPs) in mice. However, little is known about its role during gut infection in vivo. Yersinia pseudotuberculosis is an enteropathogen causing gastroenteritis, adenolymphitis and septicaemia which is able to invade its host through PPs. We investigated the role of Nod2 during Y. pseudotuberculosis infection. Death was delayed in Nod2 deleted and Crohn's disease associated Nod2 mutated mice orogastrically inoculated with Y. pseudotuberculosis. In PPs, the local immune response was characterized by a higher KC level and a more intense infiltration by neutrophils and macrophages. The apoptotic and bacterial cell counts were decreased. Finally, Nod2 deleted mice had a lower systemic bacterial dissemination and less damage of the haematopoeitic organs. This resistance phenotype was lost in case of intraperitoneal infection. We concluded that Nod2 contributes to the susceptibility to Y. pseudotuberculosis in mice.Ulrich MeinzerSophie Esmiol-WelterlinFrederick BarreauDominique BerrebiMonique DussaillantStephane BonacorsiFabrice ChareyreMichiko Niwa-KawakitaCorinne AlbertiGhislaine SterkersClaude VillardThecla LesuffleurMichel PeuchmaurMichael KarinLars EckmannMarco GiovanniniVincent OllendorffHans Wolf-WatzJean-Pierre HugotPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 7, p e2769 (2008)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Ulrich Meinzer
Sophie Esmiol-Welterlin
Frederick Barreau
Dominique Berrebi
Monique Dussaillant
Stephane Bonacorsi
Fabrice Chareyre
Michiko Niwa-Kawakita
Corinne Alberti
Ghislaine Sterkers
Claude Villard
Thecla Lesuffleur
Michel Peuchmaur
Michael Karin
Lars Eckmann
Marco Giovannini
Vincent Ollendorff
Hans Wolf-Watz
Jean-Pierre Hugot
Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
description Nucleotide oligomerisation domain 2 (NOD2) is a component of the innate immunity known to be involved in the homeostasis of Peyer patches (PPs) in mice. However, little is known about its role during gut infection in vivo. Yersinia pseudotuberculosis is an enteropathogen causing gastroenteritis, adenolymphitis and septicaemia which is able to invade its host through PPs. We investigated the role of Nod2 during Y. pseudotuberculosis infection. Death was delayed in Nod2 deleted and Crohn's disease associated Nod2 mutated mice orogastrically inoculated with Y. pseudotuberculosis. In PPs, the local immune response was characterized by a higher KC level and a more intense infiltration by neutrophils and macrophages. The apoptotic and bacterial cell counts were decreased. Finally, Nod2 deleted mice had a lower systemic bacterial dissemination and less damage of the haematopoeitic organs. This resistance phenotype was lost in case of intraperitoneal infection. We concluded that Nod2 contributes to the susceptibility to Y. pseudotuberculosis in mice.
format article
author Ulrich Meinzer
Sophie Esmiol-Welterlin
Frederick Barreau
Dominique Berrebi
Monique Dussaillant
Stephane Bonacorsi
Fabrice Chareyre
Michiko Niwa-Kawakita
Corinne Alberti
Ghislaine Sterkers
Claude Villard
Thecla Lesuffleur
Michel Peuchmaur
Michael Karin
Lars Eckmann
Marco Giovannini
Vincent Ollendorff
Hans Wolf-Watz
Jean-Pierre Hugot
author_facet Ulrich Meinzer
Sophie Esmiol-Welterlin
Frederick Barreau
Dominique Berrebi
Monique Dussaillant
Stephane Bonacorsi
Fabrice Chareyre
Michiko Niwa-Kawakita
Corinne Alberti
Ghislaine Sterkers
Claude Villard
Thecla Lesuffleur
Michel Peuchmaur
Michael Karin
Lars Eckmann
Marco Giovannini
Vincent Ollendorff
Hans Wolf-Watz
Jean-Pierre Hugot
author_sort Ulrich Meinzer
title Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
title_short Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
title_full Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
title_fullStr Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
title_full_unstemmed Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
title_sort nod2 mediates susceptibility to yersinia pseudotuberculosis in mice.
publisher Public Library of Science (PLoS)
publishDate 2008
url https://doaj.org/article/1e13e916d8c84a198cf5492130e8020a
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