Resistance to invasive pneumococcal infection in mice with acute allergic lung inflammation (MPF1P.766)

Abstract

Abstract A recent publication by Talbot et al (N Engl J Med 2005) first identified asthma as a risk factor for invasive pneumococcal disease (IPD). However, more recent reports suggest that mortality is unaffected following IPD in patients with asthma and that COPD, an obstructive condition similar to asthma, protects against the development of complicated pneumonia. To clarify the effects of asthma on the immune response to a pneumococcal infection in the lung, we used an acute murine model of ovalbumin (OVA)-induced allergic lung inflammation (ALI) and hypothesized that mice with acute ALI would show increased susceptibility to IPD. Surprisingly, mice with acute ALI demonstrated enhanced resistance to infection. Resistance in mice with ALI correlated with a greater capacity for bacterial clearance from the lungs within eight hours post infection. This early clearance resulted in decreased bacterial invasiveness into the lung tissue as well as a blunted cytokine response to infection. Despite an increase in alveolar macrophage levels following OVA challenge, the increased bacterial clearance appeared to be mediated by MHCII- SiglecF+ eosinophils. These findings suggest that while eosinophils are pathogenic in asthma they could be protective against IPD, highlighting the need for a clearer understanding of the risk of IPD in patients with different asthma phenotypes.