| MKP1 regulates the induction of inflammatory response by pneumococcal pneumolysin in human epithelial cells. | |
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MedLine Citation:
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PMID: 20868379 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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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. |
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Authors:
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Hee-Sung Shin; In-Hwa Yoo; Yong-Jae Kim; Hyong-Bai Kim; Shouguang Jin; Un-Hwan Ha |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-24 |
Journal Detail:
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Title: FEMS immunology and medical microbiology Volume: 60 ISSN: 1574-695X ISO Abbreviation: FEMS Immunol. Med. Microbiol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-02 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9315554 Medline TA: FEMS Immunol Med Microbiol Country: England |
Other Details:
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Languages: eng Pagination: 171-8 Citation Subset: IM |
Copyright Information:
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© 2010 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved. |
Affiliation:
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Department of Biotechnology and Bioinformatics, Korea University, Chungnam, Korea. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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