Dissection of a type I interferon pathway in controlling bacterial intracellular infection in mice

Cell Microbiol. 2011 Nov;13(11):1668-82. doi: 10.1111/j.1462-5822.2011.01646.x. Epub 2011 Aug 24.

Abstract

Defence mechanisms against intracellular bacterial pathogens are incompletely understood. Our study characterizes a type I IFN-dependent cell-autonomous defence pathway directed against Legionella pneumophila, an intracellular model organism and frequent cause of pneumonia. We show that macrophages infected with L. pneumophila produced IFNβ in a STING- and IRF3- dependent manner. Paracrine type I IFNs stimulated upregulation of IFN-stimulated genes and a cell-autonomous defence pathway acting on replicating and non-replicating Legionella within their specialized vacuole. Our infection experiments in mice lacking receptors for type I and/or II IFNs show that type I IFNs contribute to expression of IFN-stimulated genes and to bacterial clearance as well as resistance in L. pneumophila pneumonia in addition to type II IFN. Overall, our study shows that paracrine type I IFNs mediate defence against L. pneumophila, and demonstrates a protective role of type I IFNs in in vivo infections with intracellular bacteria.

Publication types

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

MeSH terms

  • Animals
  • Disease Models, Animal
  • Gene Expression Profiling
  • Interferon Regulatory Factor-3 / metabolism
  • Interferon Type I / immunology*
  • Legionella pneumophila / immunology*
  • Legionella pneumophila / pathogenicity*
  • Legionnaires' Disease / immunology*
  • Legionnaires' Disease / pathology*
  • Macrophages / immunology
  • Macrophages / microbiology
  • Membrane Proteins / metabolism
  • Mice
  • Signal Transduction*
  • Vacuoles / immunology
  • Vacuoles / microbiology

Substances

  • Interferon Regulatory Factor-3
  • Interferon Type I
  • Irf3 protein, mouse
  • Membrane Proteins
  • Sting1 protein, mouse