Acute inflammatory asthma protects influenza infected mice from bacterial superinfection (P3065)

Abstract

Abstract The Centers of Disease Control identified asthmatics to suffer more severe morbidity from influenza during the 2009 pandemic. However, our data indicate that pre-existing allergic inflammation during viral infection is protective against influenza associated disease in mice. Since bacterial super-infections during influenza increase morbidity and mortality, we hypothesized that acute inflammatory asthma promotes bacterial colonization of the lungs after influenza infection thereby leading to a more severe outcome. We created a triple variant model system by infecting Aspergillus fumigatus sensitized and challenged mice with 1000 TCID50/ml of A/CA/4/2009 virus a week after the last fungal challenge. Mice were co-infected with 600 cfu of Streptococcus pneumoniae strain A66.1 a week later and monitored for six days. Mice with allergic asthma lost less weight after co-infection, had less airway resistance after methacholine challenge, and had at least a 50% reduction in mortality compared to non-asthmatic controls. Fewer inflammatory cells were recruited into the airways of allergic mice after co-infection. Allergic asthma delayed S. pneumoniae colonization in the airways and lungs but not blood compared to co-infection alone. Mice in the asthma and co-infection model had less normal flora outgrowth in the airways, lungs, and blood compared to those in the co-infection model. Allergic asthma protects against, or delays, bacterial super-infection after influenza challenge.