Induction of IL-8 in periodontal ligament cells by H2O2

Journal of Microbiology - Tập 46 - Trang 579-584 - 2008
Yang-Sin Lee1, Eun Jung Bak1, Minyoung Kim1,2, Wonse Park3, Jeong Taeg Seo1,2, Yun-Jung Yoo1,2
1Department of Oral Biology, BK21 project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, Republic of Korea
2Department of Applied Life Science, The Graduate School, Yonsei University, Seoul, Republic of Korea
3Department of General Dentistry, Dental Hospital, Yonsei University, Seoul, Republic of Korea

Tóm tắt

Periodontitis is an inflammatory disease caused by bacteria. In periodontitis, reactive oxygen species (ROS) are released from inflammatory cells in response to bacteria. Interleukin (IL)-8 is one of pro-inflammatory cytokines. To investigate the role of ROS in pathogenesis of periodontitis, we estimated the effect of H2O2, one of ROS, on the expression of IL-8 in human periodontal ligament (PDL) cells. PDL cells were treated with H2O2. IL-8 expression was determined by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38) and c-jun NH2-terminal kinase (JNK) was estimated by Western blotting. Treatment with H2O2 at concentration of up to 250 μM increased IL-8 mRNA expression and production in a concentration-dependent manner. However, treatment with 500 μM H2O2 did not increase IL-8 production. Catalase, an inhibitor of H2O2, down-regulated the production of IL-8 induced by H2O2. H2O2 increased the phosphorylation of ERK, p38, and JNK. Pretreatment with PD98059 (ERK inhibitor), SB203580 (p38 inhibitor), or SP600125 (JNK inhibitor) decreased the IL-8 production induced by H2O2. These results indicate that H2O2 acts as an inducer of IL-8 secretion via activation of ERK, p38, and JNK in PDL cells. H2O2 deposited in periodontal tissue during inflammation against bacteria may accelerate tissue destruction via induction of IL-8 in PDL cells.

Tài liệu tham khảo

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