Journal of dental hygiene science (치위생과학회지)

The Korean Society of Dental Hygiene Science (한국치위생과학회)
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JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

조골세포에서 Porphyromonas gingivalis Lipopolysaccharide와 니코틴에 의한 염증에 대한 JAK/STAT Pathway의 역할

  • Han, Yang-keum (Department of Dental Hygiene, Daejeon Health Science College) ;
  • Lee, In Soo (Department of Biological Sciences and Biotechnology, College of Life Science and Nano Technology, Hannam University) ;
  • Lee, Sang-im (Department of Dental Hygiene, College of Health Sciences, Dankook University)
  • 한양금 (대전보건대학교 치위생과) ;
  • 이인수 (한남대학교 생명.나노과학대학 생명시스템과학과) ;
  • 이상임 (단국대학교 보건과학대학 치위생학과)
  • Received : 2017.01.03
  • Accepted : 2017.01.23
  • Published : 2017.02.28
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Abstract

Bacterial infection and smoking are an important risk factors involved in the development and progression of periodontitis. However, the signaling mechanism underlying the host immune response is not fully understood in periodontal lesions. In this study, we determined the expression of janus kinase (JAK)/signal transducer and activator of transcription (STAT) on Porphyromonas gingivalis lipopolysaccharide (LPS)- and nicotine-induced cytotoxicity and the production of inflammatory mediators, using osteoblasts. The cells were cultured with 5 mM nicotine in the presence of $1{\mu}g/ml$ LPS. Cell viability was determined using MTT assay. The role of JAK on inflammatory mediator expression and production, and the regulatory mechanisms involved were assessed via enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, and Western blot analysis. LPS- and nicotine synergistically induced the production of cyclooxgenase-2 (COX-2) and prostaglandin $E_2$ ($PGE_2$) and increased the protein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and $PGE_2$ as well as the expression of pro-inflammatory cytokines, such as tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$ ($IL-1{\beta}$), and IL-6 in LPS- and nicotine-stimulated osteoblasts. These results suggest that JAK/STAT is closely related to the LPS- and nicotine-induced inflammatory effects and is likely to regulate the immune response in periodontal disease associated with dental plaque and smoking.

Keywords

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