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Effect of interleukin‐17 on the expression of chemokines in gingival epithelial cells
Author(s) -
Takahashi Naoki,
Okui Takafumi,
Tabeta Koichi,
Yamazaki Kazuhisa
Publication year - 2011
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2011.00842.x
Subject(s) - interleukin 8 , chemokine , ccl2 , interleukin , secretion , inflammation , tumor necrosis factor alpha , stimulation , microbiology and biotechnology , biology , chemistry , immunology , cytokine , endocrinology
Takahashi N, Okui T, Tabeta K, Yamazaki K. Effect of interleukin‐17 on the expression of chemokines in gingival epithelial cells.
Eur J Oral Sci 2011; 119: 339–344. © 2011 Eur J Oral Sci 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.