J Dent Hyg Sci.  2017 Feb;17(1):81-86. 10.17135/jdhs.2017.17.1.81.

JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

• Han YK
• Lee IS
• Lee SI

• KMID: 2371028
• DOI: http://doi.org/10.17135/jdhs.2017.17.1.81

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 Eâ‚‚ (PGEâ‚‚) and increased the protein expression of JAK/STAT. Treatment with an JAK inhibitor blocked the production of COX-2 and PGEâ‚‚ 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.

Keyword

JAK/STAT pathway; Nicotine; Periodontitis; Porphyromonas gingivalis lipopolysaccharide

MeSH Terms

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
Cytokines
Interleukin-6
Nicotine
Phosphotransferases
Smoke