The role of type I interferons in Staphylococcus aureus infection

The importance of type I interferons (IFN) 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 gram-negative) have been shown to induce IFN-beta (IFN-beta) production in myeloid cells, but this IFN-beta is not always beneficial to the host. We examined whether Staphylococcus aureus induces IFN-beta 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-beta production compared to 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 nucleic acid ligands is essential for induction of IFN-beta and inflammatory chemokines downstream of IFN-beta. Further, we found that adding exogenous IFN-beta during S. aureus infection (in vitro and in vivo) was protective. Together, the data demonstrate that failure to induce IFN-beta production during S. aureus infection contributes to pathogenicity.