Type I Interferon Induction during Influenza Virus Infection Increases Susceptibility to Secondary Streptococcus pneumoniae Infection by Negative Regulation of γδ T Cells

摘要: The majority of deaths following influenza virus infection result from secondary bacterial superinfection, most commonly caused by Streptococcus pneumoniae. Several models have been proposed to explain how primary respiratory viral infections exacerbate disease, but the mechanistic explanations contradictory. In this study, mice were infected with S. pneumoniae at different days after A (X31) infection. Our findings show that induction type I interferons (IFNs) during a nonlethal is sufficient promote deadly Moreover, deficient in interferon receptor (IFNAR knockout [KO] mice) effectively cleared their lungs, increased recruitment neutrophils, and demonstrated an enhanced innate expression interleukin-17 (IL-17) relative wild-type (WT) mice. Lung γδ T cells responsible for almost all IL-17 production, function compromised WT not IFNAR KO Adoptive transfer reduced susceptibility lung Altogether, our study highlights importance as key master regulator exploited opportunistic pathogens such may be utilized design effective preventive therapeutic strategies beneficial coinfected patients epidemics.