Transcription profiling by array of pulmonary gene expression in response to interleukin-22 during severe influenza

Severe bacterial (pneumococcal) infections are commonly associated with influenza and are significant contributors to the excess morbidity and mortality of influenza. Disruption of lung tissue integrity during influenza participates in bacterial pulmonary colonization and dissemination out of the lungs. Interleukin (IL)-22 has gained considerable interest in anti-inflammatory and anti-infection immunotherapy over the last decade. In the current study, we investigated the effect of exogenous IL-22 delivery on the outcome of bacterial superinfection post-influenza. Our data show that exogenous treatment of influenza-infected mice with recombinant IL-22 reduces bacterial dissemination out of the lungs but is without effect on pulmonary bacterial burden. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and naïve) mice that might explain the observed effects. Indeed, exogenous IL-22 modulates gene expression profile in a way suggesting a reinforcement of tissue integrity. Our results open the way to alternative approaches for limiting post-influenza bacterial superinfection, particularly systemic bacterial invasion.