In Vitro Effects of Nicotine, Cigarette Smoke Condensate, and Porphyromonas gingivalis on Monocyte Chemoattractant Protein-1 Expression from Cultured Human Gingival Fibroblasts
- Corresponding Author:
- L. Jack Windsor, PhD
Department of Oral Biology
Indiana University School of Dentistry
1121 West Michigan Street, DS 271
Indianapolis, IN, USA 46202
E-mail: [email protected]
Received Date: January 27, 2015; Accepted Date: March 28, 2015; Published Date: April 02, 2015
Citation: Eman Allam, Mia Recupito, Hend Mohamed, L. Jack Windsor (2015) In Vitro Effects of Nicotine, Cigarette Smoke Condensate, and Porphyromonas gingivalis on Monocyte Chemoattractant Protein-1 Expression from Cultured Human Gingival Fibroblasts. J Interdiscipl Med Dent Sci 3:171. doi: 10.4172/2376-032X.1000171
Copyright: © 2015 Allam, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Monocyte chemoattractant protein-1 (MCP-1) is an inducible protein that attracts monocytes to areas of injury and infection. Studies have shown that it is produced by gingival cells in periodontal diseases and that its incidence increases with the severity of the disease. The aim of the present study was to investigate the effects of nicotine, cigarette smoke condensate (CSC), and Porphyromonas gingivalis (P. gingivalis) on MCP-1 expression from human gingival fibroblasts (HGFs) in vitro.
Methods: HGFs were exposed for 72 h to 250 µg/mL of nicotine, 100 µg/mL of CSC, 10% P. gingivalis supernatant, P. gingivalis supernatant with nicotine, or P. gingivalis supernatant with CSC. A control group comprised HGFs without any treatment. The conditioned media was then collected for MCP-1 analysis by enzyme-linked immunosorbent assay (ELISA).
Results: There were significant differences in MCP-1 level between the P. gingivalis (p=0.0432) and P. gingivalis with CSC (p=0.0037) groups when compared to the control group.
Conclusions: P. gingivalis stimulates an inflammatory response in periodontal tissues by increasing MCP-1, which helps attract host cells to combat the bacterial infection. Tobacco usage can mask the inflammatory responses normally seen in periodontal diseases by reducing the levels of MCP-1, thus allowing the bacteria to grow somewhat undetected. This could be one factor that explains why smoking is a major contributing factor to the initiation, development, and progression of periodontal diseases.