Journal of Microbiology

Journal Article

Porphyromonas gingivalis-Derived Lipopolysaccharide-Mediated Activation of MAPK Signaling Regulates Inflammatory Response and Differentiation in Human Periodontal Ligament Fibroblasts: Taegun Seo , Seho Cha , Tae-Il Kim , Hee-Jung Park , Jeong-Soon Lee , Kyung Mi Woo; J. Microbiol. 2012;50(2):311-319. Published online April 27, 2012; DOI: https://doi.org/10.1007/s12275-012-2146-x

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Porphyromonas gingivalis (P.g.), which is a potential pathogen for periodontal diseases, contains lipopolysaccharide (LPS), and this endotoxin stimulates a variety of cellular responses. At present, P.g.-derived LPS-induced cellular responses in human periodontal ligament fibroblasts (PDLFs) are not well characterized. Here, we demonstrate that P.gderived LPS regulates inflammatory responses, apoptosis and differentiation in PDLFs. Interleukin-6 (IL-6) and -8 (IL-8) were effectively upregulated by treatment of P.g.-derived LPS, and we confirmed apoptosis markers including elevated cytochrome c levels, active caspase-3 and morphological change in the presence of P.g.-derived LPS. Moreover, when PDLFs were cultured with differentiation media, P.g.- derived LPS reduced the expression of differentiation marker genes, as well as reducing alkaline phosphatase (ALP) activity and mineralization. P.g.-derived LPS-mediated these cellular responses were effectively abolished by treatment of mitogen-activated protein kinase (MAPK) inhibitors. Taken together, our results suggest that P.g.-derived LPS regulates several cellular responses via activation of MAPK signaling pathways in PDLFs.

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

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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.

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