Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL-17 and IL-22), in lungs of influenza virus-infected T-bet<sup>-/-</sup> mice, were correlated with survival advantage against subsequent infection by <i>Streptococcus pneumoniae</i> Neutralization of IL-17, but not IL-22, in T-bet<sup>-/-</sup> mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival of T-bet<sup>-/-</sup> mice.
Our data show that exogenous treatment of influenza virus-infected mice with recombinant IL-22 reduces bacterial dissemination out of the lungs but is without effect on pulmonary bacterial burden.
This study shows for the first time that a defect in IL-22 is involved in the acute exacerbation induced by NTHi infection during experimental COPD and opens the way to innovative therapeutic strategies.