Title Induction of IL-8 in Periodontal Ligament Cells by H2O2
Author Yang-Sin Lee1, Eun Jung Bak1, Minyoung Kim1,2, Wonse Park3, Jeong Taeg Seo1,2, and Yun-Jung Yoo1,2*
Address 1Department of Oral Biology, BK21 project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul 120-752, Republic of Korea, 2Department of Applied Life Science, The Graduate School, Yonsei University, Seoul 120-752, Republic of Korea, 3Department of General Dentistry, Dental Hospital, Yonsei University, Seoul 120-752, Republic of Korea
Bibliography Journal of Microbiology, 46(5),579-584, 2008,
DOI
Key Words IL-8, periodontal ligament cells, H2O2
Abstract 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.