title: Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells.
abstract: The role of interleukin (IL)-17 in cellular communication in inflammation has been well described, and a positive correlation between the severity of periodontitis and the level of IL-17 was reported. Although epithelial cells are a major target of IL-17, little is known about the effect of IL-17 on the production of chemokines by human gingival epithelial cells (HGECs). We evaluated the effects of IL-17 on the expression of CXCL8 and CCL2 by HGECs using quantitative real-time PCR and ELISA. In addition, the role of the nuclear factor (NF)-κB signalling pathway in the IL-17-mediated expression of chemokines was assessed using a specific inhibitor. Stimulation with IL-17 up-regulated the expression of CXCL8 mRNA but not of CCL2 mRNA in HGECs, whereas tumour necrosis factor-α (TNF-α) elevated the expression of mRNA for both chemokines. Stimulation with IL-17 up-regulated the secretion of CXCL8 protein, but not the secretion of CCL2 protein. The effect of IL-17 on CXCL8 production was suppressed using an anti-IL-17R Ig, suggesting a role for a specific receptor-ligand interaction. Inhibition of the NF-κB signalling pathway demonstrated that NF-κB activation is required for the CXCL8 expression in HGECs. In conclusion, IL-17 is involved in the regulation of the innate immune response in HGECs by inducing CXCL8 production.
authors: Center for Transdisciplinary Research, Niigata University, Japan.
authors: Naoki
authors: N
authors: Takahashi
authors: Takafumi
authors: T
authors: Okui
authors: Koichi
authors: K
authors: Tabeta
authors: Kazuhisa
authors: K
authors: Yamazaki
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D002460:Cell Line; D018932:Chemokine CCL2 / Q000187:drug effects*; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000187:drug effects; D005881:Gingiva / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D020381:Interleukin-17 / Q000494:pharmacology*; D016209:Interleukin-8 / Q000187:drug effects*; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D052002:NF-kappa B p50 Subunit / Q000187:drug effects; D009570:Nitriles / Q000494:pharmacology; D060888:Real-Time Polymerase Chain Reaction; D018123:Receptors, Interleukin / Q000037:antagonists & inhibitors / Q000276:immunology; D053722:Receptors, Interleukin-17 / Q000037:antagonists & inhibitors / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D013450:Sulfones / Q000494:pharmacology; D051996:Transcription Factor RelA / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: C434003:3-(4-methylphenylsulfonyl)-2-propenenitrile; D000911:Antibodies, Monoclonal; C111835:CCL2 protein, human; C508606:CXCL8 protein, human; D018932:Chemokine CCL2; C109985:IL17RA protein, human; C448419:IL17RC protein, human; D020381:Interleukin-17; D016209:Interleukin-8; D016328:NF-kappa B; D052002:NF-kappa B p50 Subunit; D009570:Nitriles; D018123:Receptors, Interleukin; D053722:Receptors, Interleukin-17; D013450:Sulfones; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha