- Induction of IL-8 in Periodontal Ligament Cells by H2O2
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Yang-Sin Lee , Eun Jung Bak , Minyoung Kim , Wonse Park , Jeong Taeg Seo , Yun-Jung Yoo
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J. Microbiol. 2008;46(5):579-584. Published online October 31, 2008
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DOI: https://doi.org/10.1007/s12275-008-0182-3
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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.
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Citations
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