Differences in responses of interleukin-1 and tumor necrosis factor α production and secretion to cyclosporin-A and ultraviolet B-irradiation by normal and transformed keratinocyte cultures.

Autor: Valère, Anne, Chardonnet, Yvette, Viac, Jacqueline, Schmitt, Daniel
Předmět:
Zdroj: Experimental Dermatology; Feb97, Vol. 6 Issue 1, p22-28, 7p
Abstrakt: Among epidermal cytokines, IL-1 and TNFα are involved in inflammatory skin reactions and suspected of modulation by immunosuppressive treatment (e.g., cyclosporin A, CsA) or UVB-irradiation, 2 mediators probably being involved in epithelial carcinogenesis. We evaluated the effects of 8 μ/ml CsA and 100 J/m[sup2] UVB-irradiation on the production and secretion of IL-1 and TNFα on normal human epidermal keratinocytes (NHK) and epidermal keratinocyte cell lines either spontaneously transformed (HaCaT) or transformed by human papillomavirus (HPV) type 16 or 18 (EK 16 and EK 18), by using ELISA test. Normal and immortalized keratinocytes constitutively produced and released IL-1α, IL-1β and IL-1 receptor antagonist (IL-1RA) but IL-1 synthesis by NHK was significantly higher than by cell lines. All the cells spontaneously excreted low amounts of TNF&alpha. Different responses to treatments were evidenced between NHK and cell lines. CsA modified significantly the production and secretion of IL-1 in most cells whereas slight changes were observed with TNFα secretion. UVB irradiation had no effect on the intracellular IL-1 pool of any cells but increased the release of IL-1 and TNFα. The association CsA-UVB did not result in additive effects on synthesis and secretion of IL-1; the release of TNFα by the cells remained poor except for EK18 cells. Taken together, these results show that, in immortalized keratinocytes, the IL-1 and TNFα expression was differently affected by treatments with CsA and/or UVB-irradiation as compared to NHK. In addition, spontaneously transformed keratinocytes. HaCaT, reacted differently from HPV-transformed keratinocytes, EK16 and EK18. [ABSTRACT FROM AUTHOR]
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