Failure to induce IFN-β production during Staphylococcus aureus infection contributes to pathogenicity.

نویسندگان

  • Amber Kaplan
  • Jun Ma
  • Pierre Kyme
  • Andrea J Wolf
  • Courtney A Becker
  • Ching Wen Tseng
  • George Y Liu
  • David M Underhill
چکیده

The importance of type I IFNs in the host response to viral infection is well established; however, their role in bacterial infection is not fully understood. Several bacteria (both Gram-positive and -negative) have been shown to induce IFN-β production in myeloid cells, but this IFN-β is not always beneficial to the host. We examined whether Staphylococcus aureus induces IFN-β from myeloid phagocytes, and if so, whether it is helpful or harmful to the host to do so. We found that S. aureus poorly induces IFN-β production compared with other bacteria. S. aureus is highly resistant to degradation in the phagosome because it is resistant to lysozyme. Using a mutant that is more sensitive to lysozyme, we show that phagosomal degradation and release of intracellular ligands is essential for induction of IFN-β and inflammatory chemokines downstream of IFN-β. Further, we found that adding exogenous IFN-β during S. aureus infection (in vitro and in vivo) was protective. Together, the data demonstrate that failure to induce IFN-β production during S. aureus infection contributes to pathogenicity.

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عنوان ژورنال:
  • Journal of immunology

دوره 189 9  شماره 

صفحات  -

تاریخ انتشار 2012