One common consequence of infection and inflammation is wasting of skeletal muscle and fat tissue. Now, a new study shows that gut colonization with the O21:H+ commensal strain of Escherichia coli can prevent wasting in a mouse model of intestinal inflammation or in mice infected with Salmonella enterica subsp. enterica serovar Typhimurium or Burkholderia thailandensis. Protection mediated by E. coli O21:H+ required bacterial translocation to the white adipose tissue (WAT) following infection or intestinal inflammation. In the WAT, E. coli O21:H+ induced high levels of insulin-like growth factor 1 (IGF1), in a process that was dependent on activation of the NLRC4 inflammasome. The high levels of IGF1 then stimulated the IGF1–phosphatidylinositol 3-kinase (PI3K)–AKT pathway in skeletal muscle, preventing muscle loss.
References
Palaferri Schieber, A. M. et al. Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling. Science 350, 558–563 (2015
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Nunes-Alves, C. Commensal bacterium prevents wasting. Nat Rev Microbiol 13, 738 (2015). https://doi.org/10.1038/nrmicro3594
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DOI: https://doi.org/10.1038/nrmicro3594