Periodontitis Research Today is a free monthly online journal that collates and summarizes the latest research about Periodontitis, including details on treatment, causes, gingivitis, symptoms. | ||||||||
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Expression of beta-defensin-2 in human gingival epithelial cells in response to challenge with Porphyromonas gingivalis in vitro.Taguchi Y, Imai H Graduate School of Dentistry (Periodontology), Osaka Dental University, Osaka, Japan. taguchi@stu.osaka-dent.ac.jp BACKGROUND AND OBJECTIVE: Human beta-defensin-2 (hBD-2) is an antimicrobial peptide that is produced by epithelial cells after stimulation with microorganisms and inflammatory mediators. Compared with gram-positive bacteria, gram-negative bacteria, which are typically detected in the periodontal pockets in periodontitis, elicit a stronger antibacterial peptide response of hBD-2 by epithelial cells. The purpose of this study was to investigate the expression of hBD-2 and relationships between it and inflammatory mediators in human gingival epithelial cells (HGEC) in response to challenge with Porphyromonas gingivalis in vitro. MATERIAL AND METHODS: mRNA expression of hBD-2 in HGEC stimulated with or without P. gingivalis was assessed using a semiquantitative reverse transcription-polymerase chain reaction. Primary cultured HGEC were activated by live P. gingivalis, and inflammatory cytokine production was examined using an enzyme-linked immunosorbent assay. RESULTS: The level of hBD-2 mRNA in HGEC treated with P. gingivalis increased with exposure time. After 48 h, the mRNA in P. gingivalis was significantly increased compared with that in control HGEC. The interleukin-8 production rate was much greater in stimulated HGEC than in the control HGEC, almost always showing a significant difference after 3 h. The production of interleukin-1beta was not increased as much as that of interleukin-8. CONCLUSION: These findings suggest that the expression of hBD-2 in HGEC is P. gingivalis-dependently induced and is likely to be connected with the initial stage of the inflammatory response. Published 10 July 2006 in J Periodontal Res, 41(4): 334-9.
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