Microbiota-derived acetate protects against respiratory syncytial virus infection through a GPR43-type 1 interferon response

Nat Commun. 2019 Jul 22;10(1):3273. doi: 10.1038/s41467-019-11152-6.

Abstract

Severe respiratory syncytial virus (RSV) infection is a major cause of morbidity and mortality in infants <2 years-old. Here we describe that high-fiber diet protects mice from RSV infection. This effect was dependent on intestinal microbiota and production of acetate. Oral administration of acetate mediated interferon-β (IFN-β) response by increasing expression of interferon-stimulated genes in the lung. These effects were associated with reduction of viral load and pulmonary inflammation in RSV-infected mice. Type 1 IFN signaling via the IFN-1 receptor (IFNAR) was essential for acetate antiviral activity in pulmonary epithelial cell lines and for the acetate protective effect in RSV-infected mice. Activation of Gpr43 in pulmonary epithelial cells reduced virus-induced cytotoxicity and promoted antiviral effects through IFN-β response. The effect of acetate on RSV infection was abolished in Gpr43-/- mice. Our findings reveal antiviral effects of acetate involving IFN-β in lung epithelial cells and engagement of GPR43 and IFNAR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • A549 Cells
  • Acetates / metabolism
  • Acetates / pharmacology*
  • Animals
  • Cell Line
  • Chlorocebus aethiops
  • Humans
  • Interferon Type I / metabolism*
  • Lung / drug effects
  • Lung / metabolism
  • Lung / virology
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microbiota*
  • Polymorphism, Single Nucleotide
  • Protective Agents / metabolism
  • Protective Agents / pharmacology
  • Receptor, Interferon alpha-beta / genetics
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / metabolism*
  • Respiratory Syncytial Virus Infections / genetics
  • Respiratory Syncytial Virus Infections / prevention & control*
  • Respiratory Syncytial Virus Infections / virology
  • Vero Cells
  • Viral Load / drug effects
  • Viral Load / genetics

Substances

  • Acetates
  • Ffar2 protein, mouse
  • Ifnar1 protein, mouse
  • Interferon Type I
  • Protective Agents
  • Receptors, G-Protein-Coupled
  • Receptor, Interferon alpha-beta