Open AccessMKP1 regulates the induction of inflammatory response by pneumococcal pneumolysin in human epithelial cells
Author(s) -
Shin HeeSung,
Yoo InHwa,
Kim YongJae,
Kim HyongBai,
Jin Shouguang,
Ha UnHwan
Publication year - 2010
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2010.00733.x
Subject(s) - pneumolysin , biology , proinflammatory cytokine , cytokine , tumor necrosis factor alpha , immunology , mapk/erk pathway , innate immune system , immune system , microbiology and biotechnology , kinase , inflammation , streptococcus pneumoniae , antibiotics
The expression of proinflammatory cytokines represents an important host innate response during infections. The reduction of cytokine expression thus mediates impaired host defenses. We previously reported that pneumococcal pneumolysin is less potent in inducing inflammatory responses in human epithelial cells at the early stage of treatment. How this might occur in response to pneumolysin is still not clearly understood. Here, we show the expression of tumor necrosis factor‐α (TNF‐α) was reduced by MAPK phosphatase 1 (MKP1), expression of which was significantly increased in response to pneumolysin at the early stage of treatment. TNF‐α expression was mediated in a time‐dependent manner by p38 mitogen‐activated protein kinase, activation of which is under the control of MKP1. Thus, this study reveals novel roles of pneumolysin in mediating MKP1 expression for the regulation of proinflammatory cytokine expression in a time‐dependent manner.