The Study Of β-defensin Inducible Expression In Human Gingival Epithelial Cells

Objective: The purpose of this study was to investigate the signaling pathwaysinvolved in human β-defensins (HBD-1,2,3) inducible expression in response to IL-1βand TNF-α in human gingival epithelial cells.Materials and methods: Healthy gingival samples were obtained from patients lessthan30years old undergoing the third-molar extraction or impacted teeth exposure indepartment of oral and maxillofacial surgery, Union Hospital. Primary humanepithelial cells were cultured by enzyme digestion method. Then the cells werepretreated with10μmol/L MAPK or NF-κB inhibitor for2hours and cultured furtherwith150ng/ml IL-1β or TNF-α. The total mRNA was extracted24hours later.Quantitative real-time PCR was utilized to quantify the HBD-1,2,3mRNAexpression.Results: HBD-1induction by IL-1β was not blocked in the presence of MAPK orNF-κB inhibitor. The HBD-1induction by TNF-α was similar to that of IL-1β. Incontrast, there was a notable decrease in HBD-2induction by IL-1β and the reductionwas81%by MAPK inhibitor and93%by NF-κB inhibitor. Similarly, the HBD-2induction by TNF-α was inhibited by76%by MAPK inhibitor and95%by NF-κBinhibitor. HBD-3induction was different from HBD-2. The HBD-3expression levelinduced by IL-1β was decreased by65%in the presence of MAPK inhibitor andinduced expression by TNF-α was decreased66%. Whereas the NF-κB inhibitorshowed no inhibition on HBD-3induction both by IL-1β and TNF-α.Conclusion: Our results suggested that different signaling pathways were involved inthe induction of human β-defensins in human gingival epithelial cells stimulated by IL-1β and TNF-α. For induced HBD-1expression by IL-1β and TNF-α, neitherMAPK nor NF-κB was essential or sufficient. Both MAPK and NF-κB signalingpathways played an important role in the HBD-2induction by IL-1β and TNF-α.Whereas the NF-κB inhibitor showed no inhibition on HBD-3induction both byIL-1β and TNF-α. Studies of the human β-defensins regulation provide information toreduce local infection and thereby reduce microbial invasion into the underlyingtissues.