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Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion

  • Author(s): Byndloss, MX
  • Olsan, EE
  • Rivera-Chávez, F
  • Tiffany, CR
  • Cevallos, SA
  • Lokken, KL
  • Torres, TP
  • Byndloss, AJ
  • Faber, F
  • Gao, Y
  • Litvak, Y
  • Lopez, CA
  • Xu, G
  • Napoli, E
  • Giulivi, C
  • Tsolis, RM
  • Revzin, A
  • Lebrilla, CB
  • Bäumler, AJ
  • et al.

Published Web Location

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642957/
No data is associated with this publication.
Abstract

© 2017, American Association for the Advancement of Science. All rights reserved. Perturbation of the gut-associated microbial community may underlie many human illnesses, but the mechanisms that maintain homeostasis are poorly understood. We found that the depletion of butyrate-producing microbes by antibiotic treatment reduced epithelial signaling through the intracellular butyrate sensor peroxisome proliferator–activated receptor g (PPAR-g). Nitrate levels increased in the colonic lumen because epithelial expression of Nos2, the gene encoding inducible nitric oxide synthase, was elevated in the absence of PPAR-g signaling. Microbiota-induced PPAR-g signaling also limits the luminal bioavailability of oxygen by driving the energy metabolism of colonic epithelial cells (colonocytes) toward b-oxidation. Therefore, microbiota-activated PPAR-g signaling is a homeostatic pathway that prevents a dysbiotic expansion of potentially pathogenic Escherichia and Salmonella by reducing the bioavailability of respiratory electron acceptors to Enterobacteriaceae in the lumen of the colon.

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