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

ABSTRACT: 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-? production in myeloid cells, but this IFN-? is not always beneficial to the host. We examined whether Staphylococcus aureus induces IFN-? 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-? 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-? and inflammatory chemokines downstream of IFN-?. Further, we found that adding exogenous IFN-? during S. aureus infection (in vitro and in vivo) was protective. Together, the data demonstrate that failure to induce IFN-? production during S. aureus infection contributes to pathogenicity.

SUBMITTER: Kaplan A 

PROVIDER: S-EPMC3478442 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature