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Influenza is an annual, global health care concern. Secondary bacterial pneumonia is a severe complication associated with primary influenza virus infection, often resulting in critical morbidity and mortality. Our laboratory has identified influenza-induced suppression of anti-bacterial Type 17 immunity as a mechanism for enhanced susceptibility to bacterial super-infection. We have shown that influenza-induced type I interferon impairs Type 17 activation. STAT1 is a transcription factor involved in interferon signaling, shared by type I, II, and III interferon. In this work, we investigated the role of STAT1 signaling during influenza, methicillin-resistant Staphylococcus aureus (MRSA) super-infection. STAT1-/- mice had increased morbidity and airway inflammation compared to control mice during influenza mono-infection. Despite this worsened anti-viral response, STAT1-/- mice were protected from super-infection bacterial burden and mortality compared to controls. Type 17 immune activation was increased in lymphocytes in STAT1-/- mice during super-infection. The elevation in Type 17 immunity was not related to increased IL-23 production, as type I interferon could inhibit IL-23 expression in a STAT1 independent manner. STAT1-/- antigen presenting cells were inherently biased towards Type 17 polarization compared to control cells. Further, STAT1-/- dendritic cells produced attenuated IL-6 and TNFα upon heat-killed S. aureus stimulation compared to control. Overall, these data indicate that STAT1 signaling plays a detrimental role in influenza, MRSA super-infection by controlling the magnitude of Type 17 immune activation.

STAT1 Is Required for Suppression of Type 17 Immunity during Influenza and Bacterial Superinfection