JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts.
10.17135/jdhs.2017.17.1.81
- Author:
Yang keum HAN
1
;
In Soo LEE
;
Sang im LEE
Author Information
1. Department of Dental Hygiene, Daejeon Health Science College, Daejeon 34504, Korea.
- Publication Type:Original Article
- Keywords:
JAK/STAT pathway;
Nicotine;
Periodontitis;
Porphyromonas gingivalis lipopolysaccharide
- MeSH:
Bacterial Infections;
Blotting, Western;
Cell Survival;
Cytokines;
Dental Plaque;
Enzyme-Linked Immunosorbent Assay;
Inflammation*;
Interleukin-6;
Necrosis;
Nicotine;
Osteoblasts*;
Periodontal Diseases;
Periodontitis;
Phosphotransferases;
Porphyromonas gingivalis*;
Porphyromonas*;
Risk Factors;
Smoke;
Smoking;
Transducers
- From:
Journal of Dental Hygiene Science
2017;17(1):81-86
- CountryRepublic of Korea
- Language:English
-
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 µg/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 E₂ (PGE₂) and increased the protein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and PGE₂ as well as the expression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β (IL-1β), 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.
