Autoinducer-2 promotes PAO1 acute lung infection the IL-17A pathway.

is an opportunistic pathogenic bacterium that causes various acute and chronic lung infections in immunocompromised patients. We previously found that a quorum sensing (QS) signal, namely, autoinducer-2 (AI-2), facilitates the pathogenicity of the wild-type (WT) PAO1 strain and . However, the immunological mechanism that leads to pulmonary injury remains to be elucidated. In this study, we aimed to investigate the effects of AI-2 on interleukin-17A (IL-17A) production during acute PAO1 lung infection using a mouse model, with an emphasis on the underlying immunological mechanism. Compared to infection with PAO1 alone, infection with PAO1 combined with AI-2 treatment resulted in significantly increased levels of IL-17A, numbers of Th17 cells and levels of STAT3 in the lung tissues of WT mice ( < 0.05), as well as more serious lung damage. In contrast, the concentrations of the proinflammatory cytokines IL-1α, IL-1β, and IL-6 and the chemokine keratinocyte-derived chemokine (KC) were significantly reduced during lung infection in IL-17A mice compared with WT mice ( < 0.05), and no effects were observed after AI-2 treatment ( > 0.05). Furthermore, the level of IL-17A in the lungs of WT mice was significantly reduced following infection with a strain harboring mutations in the QS genes and compared with the level of IL-17A following infection with PAO1. Our data suggest that AI-2 promotes PAO1 acute lung infection the IL-17A pathway by interfering with the QS systems of . IL-17A may be a therapeutic target for the treatment of acute lung infections in the clinic.