Atg7 enhances host defense against infection via downregulation of superoxide but upregulation of nitric oxide.

ABSTRACT: Pseudomonas aeruginosa is an opportunistic bacterium that can cause serious infection in immunocompromised individuals. Although autophagy may augment immune responses against P. aeruginosa infection in macrophages, the critical components and their role of autophagy in host defense are largely unknown. In this study, we show that P. aeruginosa infection-induced autophagy activates JAK2/STAT1α and increases NO production. Knocking down Atg7 resulted in increased IFN-γ release, excessive reactive oxygen species, and increased Src homology-2 domain-containing phosphatase 2 activity, which led to lowered phosphorylation of JAK2/STAT1α and subdued expression of NO synthase 2 (NOS2). In addition, we demonstrated the physiological relevance of dysregulated NO under Atg7 deficiency as atg7(-/-) m

SUBMITTER: Li X 

PROVIDER: S-EPMC4409144 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature