Effects of Methyl Gallate and Gallic Acid on the Production of Inflammatory Mediators Interleukin-6 and Interleukin-8 by Oral Epithelial Cells Stimulated with Fusobacterium nucleatum
Mi-Sun Kang1, Hee-Sook Jang2, Jong-Suk Oh1, Kyu-Ho Yang2,3, Nam-Ki Choi2,4, Hoi-Soon Lim4, and Seon-Mi Kim2,4*
1Department of Microbiology, School of Medicine, Chonnam National University, Gwangju 501-746, Republic of Korea, 2Department of Pediatric Dentistry, School of Dentistry, Chonnam National University, Gwangju 500-757, Republic of Korea, 3Brain Korea 21 Program, Chonnam National University, Gwangju 500-757, Republic of Korea, 4Dental Science Research Institute, Chonnam National University, Gwangju 500-757, Republic of Korea
Journal of Microbiology, 47(6),760-767, 2009,
methyl gallate, gallic acid, interleukin-6, interleukin-8, F. nucleatum
Interactions between periodontal bacteria and human oral epithelial cells can lead to the activation and expression of a variety of inflammatory mediators in epithelial cells. Fusobacterium nucleatum is a filamentous human pathogen that is strongly associated with periodontal diseases. This study examined the effects of methyl gallate (MG) and gallic acid (GA) on the production of inflammatory mediators, interleukin (IL)-6 and IL-8, by oral epithelial cells stimulated by F. nucleatum. In a real-time reverse transcription-polymerase chain reaction and an enzyme-linked immunosorbent assay, live F. nucleatum induced high levels of gene expression and protein release of IL-6 and IL-8. The effects of MG and GA were examined by treating KB oral epithelial cells with MG and GA and stimulating them with F. nucleatum. MG and GA inhibited significantly the increases in the IL-6 and IL-8 gene and protein levels in a dose- dependent manner. These compounds also inhibited the growth of F. nucleatum. No visible effects of MG and GA on the adhesion and invasion of KB cells by F. nucleatum were observed. In conclusion, both MG and GA inhibit IL-6 and IL-8 production from F. nucleatum-activated KB cells.