KMID : 0603820100160020119
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Journal of Experimental & Biomedical Science 2010 Volume.16 No. 2 p.119 ~ p.122
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Mycobacterium tuberculosis-induced Expression of Interleukin-1 Beta is Mediated Via Protein Kinase C Signaling Pathway
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Cho Jang-Eun
Lee Kyung-Hong Son Sin-Jee Park Sang-Jung Lee Hye-Young Kim Yoon-Suk
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Abstract
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Interleukin-1¥â (IL-1¥â) is one of the key proinflammatory cytokines and it plays an important role for the antimycobacterial host defense mechanisms. In this study, we examined Mycobacterium tuberculosis (MTB)-stimulated induction of IL-1¥â and evaluated the associated signal transduction pathways. In PMA-differentiated THP-1 cells, MTB infection increased mRNA expression of IL-1¥â in a dose-dependent manner. The expression of IL-1¥â mRNA began to be induced at 1.5 h after infection, and induced expression of IL-1¥â was retained for 48 h after MTB infection. The increase in expression of IL-1¥â caused by MTB was reduced in cells treated with Ro-31-8425 (an inhibitor of PKC¥á, ¥â¥°, ¥â¥±, ¥ã, and ¥å) or PD98059 (an inhibitor of MEK1), meanwhile, pre-treatment with Go6976 (an inhibitor of Ca ©÷?? dependent PKC¥á and PKC¥âI) or Rottlerin (an inhibitor of PKC¥ä) has no effect on MTB-induced expression of IL-1¥â mRNA. These results show that the expression of IL-1¥â mRNA caused by MTB may be mediated via MEK1 and PKC isoforms including PKC¥â¥±, PKC¥ã, or PKC¥å. Further studies are required to determine whether other PKC isoforms (PKC ¥ç, ¥è, ¥î, and ¥ë/¥é), except PKC¥ä, PKC¥á, and PKC¥âI, are also involved in IL-1¥â mRNA expression after mycobacterial infection.
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KEYWORD
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Mycobacterium tuberculosis, Interleukin-1¥â, Protein Kinase C
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