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Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion.

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
Science. 2017 357 (6351): 570-575

PMID: 28798125 · PMCID: PMC5642957 · DOI:10.1126/science.aam9949

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 γ (PPAR-γ). Nitrate levels increased in the colonic lumen because epithelial expression of , the gene encoding inducible nitric oxide synthase, was elevated in the absence of PPAR-γ signaling. Microbiota-induced PPAR-γ signaling also limits the luminal bioavailability of oxygen by driving the energy metabolism of colonic epithelial cells (colonocytes) toward β-oxidation. Therefore, microbiota-activated PPAR-γ signaling is a homeostatic pathway that prevents a dysbiotic expansion of potentially pathogenic and by reducing the bioavailability of respiratory electron acceptors to Enterobacteriaceae in the lumen of the colon.

Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

MeSH Terms (26)

Angiopoietin-like 4 Protein Anilides Animals Anti-Bacterial Agents Butyrates Caco-2 Cells Clostridium Colitis Colon Dysbiosis Enterobacteriaceae Epithelial Cells Female Gastrointestinal Microbiome Gene Expression Homeostasis Humans Male Mice Mice, Inbred C57BL Nitrates Nitric Oxide Synthase Type II Oxidation-Reduction PPAR gamma Signal Transduction Streptomycin

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