| First Author | Yue L | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 533 |
| Issue | 3 | Pages | 296-303 |
| PubMed ID | 32958258 | Mgi Jnum | J:304528 |
| Mgi Id | MGI:6693985 | Doi | 10.1016/j.bbrc.2020.09.032 |
| Citation | Yue L, et al. (2020) PTP1B negatively regulates STAT1-independent Pseudomonas aeruginosa killing by macrophages. Biochem Biophys Res Commun 533(3):296-303 |
| abstractText | 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-beta and interferon gamma-inducible protein 10 (CXCL10, IP-10). Unexpectedly, the phosphorylation level of STAT1 was not regulated by PTP1B. In vivo experiments also confirmed that the regulatory function of PTP1B was not dependent on STAT1. These findings demonstrate that STAT1 is dispensable for negative regulation of P. aeruginosa clearance by macrophages. |
