LAUSR

&NA; Post‐viral pneumococcal pneumonia is a leading morbidity and mortality in older patients (≥65 years of age). The goal of our current study is to understand the impact of chronological aging on innate immune responses to a secondary, post viral infection with Streptococcus pneumoniae, a causative agent of bacterial pneumonia. Using aged murine models of infection, our findings demonstrate increased morbidity and mortality in aged mice within 48 h post‐secondary S. pneumoniae infection. Increased susceptibility of aged mice was associated with decreased TLR1, TLR6, and TLR9 mRNA expression and diminished IL1&bgr; mRNA expression. Examination of NLRP3 inflammasome expression illustrated decreased NLRP3 mRNA expression and decreased IL1&bgr; production in aged lung in response to secondary S. pneumoniae infection. HighlightsOur study was designed to understand the impact of chronological aging on innate immune responses to a secondary, post influenza infection.Increased susceptibility of aged mice to secondary S. pneumoniae infection was associated with decreased IL1&bgr; mRNA expression.Examination of NLRP3 inflammasome expression illustrated decreased IL1&bgr; production in aged lung in response to secondary infection.