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Journal of Dental Research
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Biological

Regulation of CXCL9/10/11 in Oral Keratinocytes and Fibroblasts

K. Ohta*, H. Shigeishi, M. Taki, H. Nishi, K. Higashikawa, M. Takechi and N. Kamata

Department of Oral and Maxillofacial Surgery, Division of Cervico-Gnathostomatology, Programs for Applied Biomedicine, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima 734-8553, Japan;

Correspondence: * corresponding author, otkouji{at}hiroshima-u.ac.jp

Th1 and Th2 cytokines such as interferon-{gamma} (IFN-{gamma} ) , tumor necrosis factor- {alpha} (TNF-{alpha} ), and IL-4 are expressed in T-cell-mediated inflammation in the oral cavity. We tested the hypothesis that those cytokines may act on CXCR3-agonistic chemokines, T-cell recruiting factors, and on neighboring cells, including oral keratinocytes and fibroblasts. Human immortalized oral keratinocytes (RT7) and fibroblasts (GT1) after 24-hour stimulation with IFN-{gamma} showed increased mRNA levels of CXCL9 (600- and 700-fold), CXCL10 (10,000- and 150-fold), and CXCL11 (5000- and 300-fold), respectively. In contrast, TNF-{alpha} caused an increase in CXCL9 (300-fold), CXCL10 (2000-fold), and CXCL11 (2000-fold) mRNA levels in GT1, but not RT7 cells, at 24 hrs. IL-4 reinforced the promotion of CXCL9, CXCL10, and CXCL11 expression by IFN-{gamma} in RT7 cells, whereas IL-4 inhibited the increased levels by IFN-{gamma} and TNF-{alpha} in GT1 cells. Thus, IFN-{gamma} , TNF-{alpha} , and IL-4 appear cooperatively to regulate CXCR3-agonistic chemokines in oral keratinocytes and fibroblasts in T-cell-mediated oral inflammation sites.

Key Words: Chemokine • oral keratinocytes • oral fibroblasts • Th1 cytokine • Th2 cytokine

Journal of Dental Research, Vol. 87, No. 12, 1160-1165 (2008)
DOI: 10.1177/154405910808701211
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