期刊
PATHOGENS AND DISEASE
卷 71, 期 1, 页码 65-68出版社
OXFORD UNIV PRESS
DOI: 10.1111/2049-632X.12115
关键词
Rothia dentocariosa; inflammation; TNF-alpha; Toll-like receptor 2
资金
- Private University High Technology Research Center Project [S1001010]
- [21791796]
- [22592048]
- Grants-in-Aid for Scientific Research [25861750] Funding Source: KAKEN
Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-alpha in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R.dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-alpha in a dose-dependent manner. The bacterial induction of TNF-alpha in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-alpha in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-kappa B activation by R.dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-kappa B-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-kappa B activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-kappa B activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R.dentocariosa induces host TNF-alpha production by a TLR2-dependent mechanism.
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