Editors' ChoiceHost-Microbe Interactions

Respiring with H2O2

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Science Signaling  12 Jan 2021:
Vol. 14, Issue 665, eabg4522
DOI: 10.1126/scisignal.abg4522

Intestinal microbes exploit host-derived H2O2 for respiration under both normal and inflammatory conditions.

Under normal conditions, the intestinal lumen is hypoxic, which favors the growth of anaerobic commensal bacteria and restricts the growth of aerobic pathogens and opportunistic pathogens, and relatively low in host-produced antimicrobial reactive oxygen species (ROS), such as H2O2. Changes in O2 availability or inflammation drive intestinal dysbiosis (see Crowley and Vallance). Chanin et al. and Miller et al. report that Enterobacteriaceae used colonocyte-derived H2O2 to gain a growth advantage over other bacteria in the mouse gut. Chanin et al. found that the cytochrome bd oxidase AppBCX was required for a human commensal strain of the facultative anaerobe Escherichia coli, which is present in the gut under normal conditions but can overgrow when the gut is inflamed, to aerobically respire during gut inflammation. During chemically induced colitis, wild-type E. coli outcompeted appC mutants in the gut, but not if the intestinal epithelium lacked the NADPH oxidase NOX1, which produces ROS that are subsequently converted to H2O2. Results from experiments in vitro and in vivo were consistent with the catalases KatE and KatG mediating the conversion of H2O2 to the O2 used for AppC-dependent respiration, demonstrating how this bacterium could use host-derived H2O2 for aerobic respiration. Although H2O2 is generally low throughout the noninflamed intestine, it is present at the epithelial surface in the colon (see Crowley and Vallance). Miller et al. found that the murine pathogen Citrobacter rodentium, which attaches to the intestinal epithelium using a type III secretion system (T3SS), used host-produced H2O2 to drive aerobic respiration. Mutant bacteria lacking a functional T3SS or Ccp were outcompeted by wild-type cells in the mouse gut and were unable to colonize mice lacking the epithelial enzyme NOX1, though they were able to colonize mice lacking the phagocytic enzyme NOX2. Together, these studies demonstrate how microbes can exploit epithelium-produced H2O2 for a growth advantage during both normal and inflammatory conditions.

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