FIP200 is involved in murine pseudomonas infection by regulating HMGB1 intracellular translocation.

摘要: c The first two authors contributed equally to this work Abstract Background: FIP200, a critical autophagy initiating protein, can participate in numerous cellular functions including cancer development; however, its functional role P. aeruginosa infection of alveolar macrophages is unknown. Methods: To investigate the FIP200 host defense, we transfected murine macrophage MH-S cells with siRNA. Having confirmed that knockdown inhibited PAO1-induced autophagosme formation, sought characterize underlying signaling pathways by immunoblotting. Further, used fip200 KO mice study effects deficiency on HMGB1 translocation. Results: We showed Pseudomonas PAO1 strain facilitated autophagosome whereas formation and expression cells. Silencing impaired translocation cytosol almost abolished acetylation during infection. In contrast, overexpression from nuclei increased PAO1-infected Importantly, were also significantly down-regulated following Conclusions: Collectively, these findings elucidate may regulate infection, which indicate novel therapeutic targets control pulmonary