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자료유형
학술저널
저자정보
저널정보
한국치위생과학회 치위생과학회지 치위생과학회지 제17권 제1호
발행연도
2017.1
수록면
81 - 86 (6page)

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Bacterial infection and smoking are an important risk factors involved in the development and progression of periodontitis. However, the signalingmechanism underlying the host immune response is not fully understood in periodontal lesions. In this study, we determined the expression of januskinase (JAK)/signal transducer and activator of transcription (STAT) on Porphyromonas gingivalis lipopolysaccharide (LPS)- and nicotine-inducedcytotoxicity and the production of inflammatory mediators, using osteoblasts. The cells were cultured with 5 mM nicotine in the presence of 1 μg/mlLPS. Cell viability was determined using MTT assay. The role of JAK on inflammatory mediator expression and production, and the regulatorymechanisms involved were assessed via enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blotanalysis. LPS- and nicotine synergistically induced the production of cyclooxgenase-2 (COX-2) and prostaglandin E2 (PGE2) and increased theprotein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and PGE2 as well as the expression ofpro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-6 in LPS- and nicotine-stimulated osteoblasts. Theseresults suggest that JAK/STAT is closely related to the LPS- and nicotine-induced inflammatory effects and is likely to regulate the immune responsein periodontal disease associated with dental plaque and smoking.

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