ArticlePloS one2008
Nod2 mediates susceptibility to Yersinia pseudotuberculosis in mice.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Crohn's Disease: Is the Cold Chain Hypothesis Still Hot?Journal of Crohn's & colitis · 2021Review
- Editorial: The Pathogenic Yersiniae-Advances in the Understanding of Physiology and Virulence, Second Edition.Frontiers in cellular and infection microbiology · 2019Article
- Prevalence ofFrontiers in cellular and infection microbiology · 2018Article
- Microbiota Composition and Immune Responses DuringEuropean journal of microbiology & immunology · 2017Article
- Nod2: The intestinal gate keeper.PLoS pathogens · 2017Review
- Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease inFrontiers in cellular and infection microbiology · 2017Article
- Article
- Immune responses uponGut pathogens · 2017Article
- Nucleotide-binding oligomerization domain-containing protein 2 controls host response to Campylobacter jejuni in Il10-/- mice.The Journal of infectious diseases · 2014Article
- Colonization of cecum is important for development of persistent infection by Yersinia pseudotuberculosis.Infection and immunity · 2014Article
- NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection.Autophagy · 2014Article
- Nucleotide-binding oligomerization domain 2 signaling promotes hyperresponsive macrophages and colitis in IL-10-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Nucleotide-binding oligomerization domain 2 (Nod2) is dispensable for the innate immune responses of macrophages against Yersinia enterocolitica.Journal of microbiology (Seoul, Korea) · 2012Article
- In vivo-induced InvA-like autotransporters Ifp and InvC of Yersinia pseudotuberculosis promote interactions with intestinal epithelial cells and contribute to virulence.Infection and immunity · 2012Article
- Host genetics and environmental factors regulate ecological succession of the mouse colon tissue-associated microbiota.PloS one · 2012Article
- Expression and functional importance of innate immune receptors by intestinal epithelial cells.Cellular and molecular life sciences : CMLS · 2011Review
- NOD1 and NOD2 regulation of pulmonary innate immunity to Legionella pneumophila.European journal of immunology · 2010Article
- Direct bacterial killing in vitro by recombinant Nod2 is compromised by Crohn's disease-associated mutations.PloS one · 2010Article
- MDP-NOD2 stimulation induces HNP-1 secretion, which contributes to NOD2 antibacterial function.Inflammatory bowel diseases · 2010Article
- NOD2 mutations and anti-Saccharomyces cerevisiae antibodies are risk factors for Crohn's disease in African Americans.The American journal of gastroenterology · 2010Article
Corrections and comments
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Authors and funding
19 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.