English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Infections, microbe sampling and occasional leakage of commensal microbiota and their products across the intestinal epithelial cell layer represent a permanent challenge to the intestinal immune system. The production of reactive oxygen species by NADPH oxidase is thought to be a key element of defense. Patients suffering from chronic granulomatous disease are deficient in one of the subunits of NADPH oxidase. They display a high incidence of Crohn’s disease-like intestinal inflammation and are hyper-susceptible to infection with fungi and bacteria, including a 10-fold increased risk of Salmonellosis. It is not completely understood which steps of the infection process are affected by the NADPH oxidase deficiency. We employed a mouse model for  Salmonella  diarrhea to study how NADPH oxidase deficiency ( Cybb   −/− ) affects microbe handling by the large intestinal mucosa. In this animal model, wild type  S . Typhimurium causes pronounced enteropathy in wild type mice. In contrast, an avirulent  S . Typhimurium mutant ( S .Tm avir ;  invGsseD ), which lacks virulence factors boosting trans-epithelial penetration and growth in the lamina propria, cannot cause enteropathy in wild type mice. We found that  Cybb   −/−  mice are efficiently infected by  S .Tm avir  and develop enteropathy by day 4 post infection. Cell depletion experiments and infections in  Cybb   −/−   Myd88   −/−  mice indicated that the  S .Tm avir -inflicted disease in  Cybb   −/−  mice hinges on CD11c + CX 3 CR1 +  monocytic phagocytes mediating colonization of the cecal lamina propria and on  Myd88 -dependent proinflammatory immune responses. Interestingly, in mixed bone marrow chimeras a partial reconstitution of C ybb -proficiency in the bone marrow derived compartment was sufficient to ameliorate disease severity. Our data indicate that NADPH oxidase expression is of key importance for restricting the growth of  S .Tm avir  in the mucosal lamina propria. This provides important insights into microbe handling by the large intestinal mucosa and the role of NADPH oxidase in maintaining microbe-host mutualism at this exposed body surface.

plos one

NADPH Oxidase Deficient Mice Develop Colitis and Bacteremia upon Infection with Normally Avirulent, TTSS-1- and TTSS-2-Deficient Salmonella Typhimurium