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Chlamydia psittaci inhibits apoptosis of human neutrophils by activating P2X7 receptor expression
Affiliation:1. Institute of Pathogenic Biology, Hengyang Medical School, University of South China, Hengyang, Hunan, China;2. Department of Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang, Hunan, China;3. The First Affiliated Hospital, Hengyang Medical School, University of South China, Hunan, China;4. The Affiliated Nanhua Hospital, Department of laboratory medicine, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China
Abstract:This study tested the hypothesis that Chlamydia psittaci (C. psittaci) survives and multiplies in human neutrophils by activating P2X7, a nonselective cationic channel receptor expressed constitutively on the surface of these cells. Findings illustrated that P2X7 receptor expression was enhanced in C. psittaci-infected neutrophils. C. psittaci was able to inhibite spontaneous apoptosis of neutrophils through mitochondrial-induced ATP release and IL-8 production. Importantly, inhibiting ATP activation of the P2X7 receptor with AZ10606120 promotes apoptosis, while stimulating P2X7 receptor expression with BzATP delayed spontaneous apoptosis of human neutrophils, suggesting that C. psittaci inhibits apoptosis of human neutrophils by activating P2X7 receptor. This study reveals new insights into the survival advantages of the latent persistent state of C. psittaci and the mechanism by which it evades the innate immune response.
Keywords:Human neutrophils  Apoptosis  P2X7 receptor  Immune evasion  IL-8
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