Commensal bacteria calibrate the activation threshold of innate antiviral immunity

Immunity. 2012 Jul 27;37(1):158-70. doi: 10.1016/j.immuni.2012.04.011. Epub 2012 Jun 14.

Abstract

Signals from commensal bacteria can influence immune cell development and susceptibility to infectious or inflammatory diseases. However, the mechanisms by which commensal bacteria regulate protective immunity after exposure to systemic pathogens remain poorly understood. Here, we demonstrate that antibiotic-treated (ABX) mice exhibit impaired innate and adaptive antiviral immune responses and substantially delayed viral clearance after exposure to systemic LCMV or mucosal influenza virus. Furthermore, ABX mice exhibited severe bronchiole epithelial degeneration and increased host mortality after influenza virus infection. Genome-wide transcriptional profiling of macrophages isolated from ABX mice revealed decreased expression of genes associated with antiviral immunity. Moreover, macrophages from ABX mice exhibited defective responses to type I and type II IFNs and impaired capacity to limit viral replication. Collectively, these data indicate that commensal-derived signals provide tonic immune stimulation that establishes the activation threshold of the innate immune system required for optimal antiviral immunity.

Publication types

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

MeSH terms

  • Adaptive Immunity
  • Animals
  • Anti-Bacterial Agents / pharmacology
  • Arenaviridae Infections / genetics
  • Arenaviridae Infections / immunology
  • Bacteria / drug effects
  • Bacteria / immunology*
  • Disease Susceptibility / immunology
  • Immunity, Innate*
  • Interferons / immunology
  • Lymphocytic choriomeningitis virus / immunology
  • Macrophages / immunology
  • Macrophages / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Orthomyxoviridae / immunology
  • Orthomyxoviridae Infections / genetics
  • Orthomyxoviridae Infections / immunology
  • Viruses / immunology*

Substances

  • Anti-Bacterial Agents
  • Interferons

Grants and funding