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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2010.6
- 수록면
- 119 - 122 (4page)
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Interleukin-1β (IL-1β) 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-1β and evaluated the associated signal transduction pathways. In PMA-differentiated THP-1 cells, MTB infection increased mRNA expression of IL-1β in a dose-dependent manner. The expression of IL-1β mRNA began to be induced at 1.5 h after infection, and induced expression of IL-1β was retained for 48 h after MTB infection. The increase in expression of IL-1β caused by MTB was reduced in cells treated with Ro-31-8425 (an inhibitor of PKCα, βⅠ, βⅡ, γ, and ε) or PD98059 (an inhibitor of MEK1), meanwhile, pre-treatment with Go6976 (an inhibitor of Ca ²?? dependent PKCα and PKCβI) or Rottlerin (an inhibitor of PKCδ) has no effect on MTB-induced expression of IL-1β mRNA. These results show that the expression of IL-1β mRNA caused by MTB may be mediated via MEK1 and PKC isoforms including PKCβⅡ, PKCγ, or PKCε. Further studies are required to determine whether other PKC isoforms (PKC η, θ, ξ, and λ/ι), except PKCδ, PKCα, and PKCβI, are also involved in IL-1β mRNA expression after mycobacterial infection.
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UCI(KEPA) : I410-ECN-0101-2010-510-002463698