Resistance to invasive pneumococcal infection in mice with acute allergic lung inflammation (P3228)

Abstract

Abstract Streptococcus pneumoniae is the most common cause of bacterial pneumonia which results in 175,000 hospitalizations as well as 40,000 deaths in the United States annually. Recent work has identified a link between asthma and invasive pneumococcal disease (IPD) prompting the Advisory Committee on Immunization Practices to recommend that all adults with asthma receive vaccination. To study the underlying mechanism responsible for an increased risk of IPD for individuals with asthma, we used an acute model of ovalbumin (OVA)-induced allergic lung inflammation (ALI) and hypothesized that mice with acute ALI would be more susceptible than naive mice to a pulmonary S. pneumoniae infection. Surprisingly, mice with acute ALI were more resistant to infection than naïve controls and this increased resistance was found to be greatest 10 days following the final OVA challenge. While inflammatory cell infiltration and cytokine levels in the bronchoalveolar lavage (BAL) fluid had returned to levels similar to naïve controls by day 10, this time point also correlated with the peak of IgA expression in the BAL fluid, suggesting a critical role for non-specific IgA in protection against IPD. Indeed, protection against IPD was lost in IgA KO mice with ALI as well as naïve IgA KO mice.