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Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling.


ABSTRACT: Infections and inflammation can lead to cachexia and wasting of skeletal muscle and fat tissue by as yet poorly understood mechanisms. We observed that gut colonization of mice by a strain of Escherichia coli prevents wasting triggered by infections or physical damage to the intestine. During intestinal infection with the pathogen Salmonella Typhimurium or pneumonic infection with Burkholderia thailandensis, the presence of this E. coli did not alter changes in host metabolism, caloric uptake, or inflammation but instead sustained signaling of the insulin-like growth factor 1/phosphatidylinositol 3-kinase/AKT pathway in skeletal muscle, which is required for prevention of muscle wasting. This effect was dependent on engagement of the NLRC4 inflammasome. Therefore, this commensal promotes tolerance to diverse diseases.

SUBMITTER: Schieber AM 

PROVIDER: S-EPMC4732872 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling.

Schieber Alexandria M Palaferri AM   Lee Yujung Michelle YM   Chang Max W MW   Leblanc Mathias M   Collins Brett B   Downes Michael M   Evans Ronald M RM   Ayres Janelle S JS  

Science (New York, N.Y.) 20151001 6260


Infections and inflammation can lead to cachexia and wasting of skeletal muscle and fat tissue by as yet poorly understood mechanisms. We observed that gut colonization of mice by a strain of Escherichia coli prevents wasting triggered by infections or physical damage to the intestine. During intestinal infection with the pathogen Salmonella Typhimurium or pneumonic infection with Burkholderia thailandensis, the presence of this E. coli did not alter changes in host metabolism, caloric uptake, o  ...[more]

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