Immune predisposition drives susceptibility to pneumococcal pneumonia after mild influenza A virus infection in mice

Introduction A frequent sequela of influenza virus (IAV) infection is secondary bacterial pneumonia. Therefore, it clinically important to understand the genetic predisposition IAV and coinfection. Methods BALB/c C57BL/6 (B6) mice were infected with high or low-pathogenic Streptococcus pneumoniae ( SPn ). The contribution cellular molecular immune factors resistance/susceptibility B6 dissected in nonlethal lethal IAV/ coinfection models. Results Low-virulent X31 (H3N2) rendered extremely susceptible superinfection, while remained unaffected. alone barely induces IFN-γresponse two strains mice; however, superinfection significantly enhances IFN-γ production mice. As a result, signaling inhibits neutrophil recruitment clearance, leading X31/ Conversely, diminished competent responses enable highly resistant X31/SPn Discussion results establish that type 1 plays key role susceptibility pneumococcal pneumonia after mild infection.