Abstract
Staphylococcus aureus is a leading cause of pneumonia with much of the disease caused by the host response. We hypothesized the host would differentially respond to a strain of S. aureus that is a well characterized commensal (502A) compared to USA300, a major cause of respiratory, skin and soft tissue infections that is currently epidemic in the United States. As predicted, 502A was less invasive than USA300 in invasion of several skin and airway epithelial cell lines. We observed a significant increase in the type I interferon (IFN) response to 502A compared to USA300 in epithelial (107-fold, P P P P P P P P P Ifnar −/− mice. These results indicate that multiple mechanisms exist to sense bacteria within a given species and highlight a difference in host signaling between virulent and commensal strains.
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