Type I interferon production enhances susceptibility to Listeria monocytogenes infection

Ryan M. O'Connell, Supriya K. Saha, Sagar A. Vaidya, Kevin W. Bruhn, Gustavo A. Miranda, Brian Zarnegar, Andrea K. Perry, Bidong O. Nguyen, Timothy F Lane, Tadatsugu Taniguchi, Jeff F. Miller, Genhong Cheng*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

372 Scopus citations

Abstract

Numerous bacterial products such as lipopolysaccharide potently induce type I interferons (IFNs); however, the contribution of this innate response to host defense against bacterial infection remains unclear. Although mice deficient in either IFN regulatory factor (IRF)3 or the type I IFN receptor (IFNAR)1 are highly susceptible to viral infection, we show that these mice exhibit a profound resistance to infection caused by the Gram-positive intracellular bacterium Listeria monocytogenes compared with wild-type controls. Furthermore, this enhanced bacterial clearance is accompanied by a block in L. monocytogenes-induced splenic apoptosis in IRF3- and IFNAR1-deficient mice. Thus, our results highlight the disparate roles of type I IFNs during bacterial versus viral infections and stress the importance of proper IFN modulation in host defense.

Original languageEnglish (US)
Pages (from-to)437-445
Number of pages9
JournalJournal of Experimental Medicine
Volume200
Issue number4
DOIs
StatePublished - Aug 16 2004

Keywords

  • Apoptosis
  • IFN target gene
  • IFNAR
  • IRF3
  • Intracellular bacteria

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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