Loss of T-bet confers survival advantage to influenza-bacterial superinfection.

ABSTRACT: The transcription factor, T-bet, regulates type 1 inflammatory responses against a range of infections. Here, we demonstrate a previously unaddressed role of T-bet, to influenza virus and bacterial superinfection. Interestingly, we found that T-bet deficiency did not adversely affect the efficacy of viral clearance or recovery compared to wild-type hosts. Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL-17 and IL-22), in lungs of influenza virus-infected T-bet^-/- mice, were correlated with survival advantage against subsequent infection by Streptococcus pneumoniae Neutralization of IL-17, but not IL-22, in T-bet^-/- mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival

SUBMITTER: Er JZ 

PROVIDER: S-EPMC6315292 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature