PTP1B negatively regulates STAT1-independent Pseudomonas aeruginosa killing by macrophages.

Pseudomonas aeruginosa is the main conditional pathogen of immunodeficiency individuals. The mechanisms governing immune response to P. aeruginosa infection by macrophages remain incompletely defined. Herein, we demonstrate that protein tyrosine phosphatase-1B (PTP1B) is a critical negative regulator of P. aeruginosa infection response by macrophages. PTP1B-deficient macrophages display greatly enhanced bacterial phagocytosis and killing, accompanied by increased lysosome formation during P. aeruginosa infection. We also found that PTP1B repressed nitric oxide (NO) production and nitric oxide synthase (iNOS) induction following P. aeruginosa infection. PTP1B deficiency tended to upregulate the production of TRIF-interferon (IFN) pathway cytokines and chemokines, including IFN-β and interferon γ-inducible protein 10 (CXCL10, IP-10). Unexpectedly, the phosphorylation level of was not regulated by PTP1B. In vivo experiments also confirmed that the regulatory function of PTP1B was not dependent on These findings demonstrate that duanyu18131 is dispensable for negative regulation of P. aeruginosa clearance by macrophages.

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