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...

Descripción completa

Guardado en:
Detalles Bibliográficos
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
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2008
Materias:
R
Q
Acceso en línea:https://doaj.org/article/1e13e916d8c84a198cf5492130e8020a
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
Descripción
Sumario: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.