GPR43 mediates microbiota metabolite SCFA regulation of antimicrobial peptide expression in intestinal epithelial cells via activation of mTOR and STAT3

Mucosal Immunol. 2018 May;11(3):752-762. doi: 10.1038/mi.2017.118. Epub 2018 Feb 7.

Abstract

The antimicrobial peptides (AMP) produced by intestinal epithelial cells (IEC) play crucial roles in the regulation of intestinal homeostasis by controlling microbiota. Gut microbiota has been shown to promote IEC expression of RegIIIγ and certain defensins. However, the mechanisms involved are still not completely understood. In this report, we found that IEC expression levels of RegIIIγ and β-defensins 1, 3, and 4 were lower in G protein-coupled receptor (GPR)43-/- mice compared to that of wild-type (WT) mice. Oral feeding with short-chain fatty acids (SCFA) promoted IEC production of RegIIIγ and defensins in mice. Furthermore, SCFA induced RegIIIγ and β-defensins in intestinal epithelial enteroids generated from WT but not GPR43-/- mice. Mechanistically, SCFA activated mTOR and STAT3 in IEC, and knockdown of mTOR and STAT3 impaired SCFA induction of AMP production. Our studies thus demonstrated that microbiota metabolites SCFA promoted IEC RegIIIγ and β-defensins in a GPR43-dependent manner. The data thereby provide a novel pathway by which microbiota regulates IEC expression of AMP and intestinal homeostasis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Infective Agents / metabolism
  • Fatty Acids, Volatile / metabolism
  • Gastrointestinal Microbiome / physiology*
  • Homeostasis
  • Immunity, Innate
  • Intestinal Mucosa / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Pancreatitis-Associated Proteins / genetics
  • Pancreatitis-Associated Proteins / metabolism
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / metabolism*
  • STAT3 Transcription Factor / metabolism
  • TOR Serine-Threonine Kinases / metabolism
  • beta-Defensins / genetics
  • beta-Defensins / metabolism

Substances

  • Anti-Infective Agents
  • Fatty Acids, Volatile
  • Ffar2 protein, mouse
  • Pancreatitis-Associated Proteins
  • Receptors, G-Protein-Coupled
  • Reg3g protein, mouse
  • STAT3 Transcription Factor
  • beta-Defensins
  • mTOR protein, mouse
  • TOR Serine-Threonine Kinases