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Infect Immun. 2018 Apr 16. pii: IAI.00706-17. doi: 10.1128/IAI.00706-17. [Epub ahead of print]
Interleukin-22 immunotherapy during severe influenza enhances lung tissue integrity and reduces secondary bacterial systemic invasion.
Barthelemy A1,2,3,4,5, Sencio V1,2,3,4,5, Soulard D1,2,3,4,5, Deruyter L1,2,3,4,5, Faveeuw C1,2,3,4,5, Le Goffic R6, Trottein F7,2,3,4,5.
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Abstract
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 pneumococcal 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. Reduced systemic bacterial dissemination was linked to reinforced pulmonary barrier functions, as revealed by total protein measurement in the bronchoalveolar fluids, intratracheal fluorescein isothiocyanate-dextran tracking and histological approaches. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and na?ve) 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.
PMID: 29661933 DOI: 10.1128/IAI.00706-17
Interleukin-22 immunotherapy during severe influenza enhances lung tissue integrity and reduces secondary bacterial systemic invasion.
Barthelemy A1,2,3,4,5, Sencio V1,2,3,4,5, Soulard D1,2,3,4,5, Deruyter L1,2,3,4,5, Faveeuw C1,2,3,4,5, Le Goffic R6, Trottein F7,2,3,4,5.
Author information
Abstract
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 pneumococcal 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. Reduced systemic bacterial dissemination was linked to reinforced pulmonary barrier functions, as revealed by total protein measurement in the bronchoalveolar fluids, intratracheal fluorescein isothiocyanate-dextran tracking and histological approaches. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and na?ve) 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.
PMID: 29661933 DOI: 10.1128/IAI.00706-17