| First Author | Byndloss MX | Year | 2017 |
| Journal | Science | Volume | 357 |
| Issue | 6351 | Pages | 570-575 |
| PubMed ID | 28798125 | Mgi Jnum | J:244637 |
| Mgi Id | MGI:5913416 | Doi | 10.1126/science.aam9949 |
| Citation | Byndloss MX, et al. (2017) Microbiota-activated PPAR-gamma signaling inhibits dysbiotic Enterobacteriaceae expansion. Science 357(6351):570-575 |
| abstractText | 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 gamma (PPAR-gamma). 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-gamma signaling. Microbiota-induced PPAR-gamma signaling also limits the luminal bioavailability of oxygen by driving the energy metabolism of colonic epithelial cells (colonocytes) toward beta-oxidation. Therefore, microbiota-activated PPAR-gamma 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. |
