期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 186, 期 5, 页码 1234-1244出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2016.01.005
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资金
- Natural Science Foundation of China [81471564]
- Natural Sciences and Engineering Research Council of Canada
- Yunnan Natural Science Foundation [2013FZ135]
- Jeanne and Jean-Louis Levesque Chair in Cancer Research grant
Pseudomonas aeruginosa is a major opportunistic pathogen in immune-compromised individuals. Mechanisms governing immune responses to P. aeruginosa infection remain incompletely defined. Herein, we demonstrate that protein tyrosine phosphatase-1B (PTP1B) is a critical negative regulator in P. aeruginosa. infection. PTP1B-deficient mice display greatly enhanced bacterial clearance and reduced disease scores, which are accompanied by increased neutrophil infiltration and cytokine production. Interestingly, PTP1B deficiency mainly up-regulates the production of interferon-stimulated response elements regulated cytokines and chemokines, including chemokine Ligand 5 (regulated on activation normal T cell expressed and secreted), CXCL10 (interferon gamma-inducible protein 10), and interferon-beta production. Further studies reveal that PTP1B deficiency leads to increased interferon regulatory factor 7 (IRF7) expression and activation. These findings demonstrate a novel regulatory mechanism of the immune response to P. aeruginosa infection through PTP1B-IRF7 interaction. This novel PTP1B-IRF7-interferon-stimulated response elements pathway may have broader implications in Toll-like receptor-mediated innate immunity.
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