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Inhibition of ultraviolet B radiation-induced interleukin 10 expression in murine keratinocytes by selenium compounds
T S Rafferty1, C Walker, J A A Hunter
1Department of Dermatology, University of Edinburgh, Royal Infirmary of Edinburgh, Lauriston Building, Edinburgh EH3 9YW, UK.
Background:
Selenium is an essential trace nutrient necessary for the normal function of the immune system. Selenium compounds protect mice against ultraviolet (UV) B-induced tumours, probably by preventing oxidative damage to the host skin cells and to the host immune system. One possible mechanism of protection is that selenium can prevent oxidative stress-induced release of cytokines such as interleukin (IL)-10, which could suppress cell-mediated immunity.
Objectives:
To determine whether selenium compounds can inhibit UVB induction of IL-10 protein in murine keratinocytes.
Methods:
The murine keratinocyte cell line PAM 212 was treated with or without selenomethionine (50-200 nmol L-1) or sodium selenite (1-50 nmol L(-1)) for 24 h before exposure to 200 J m(-2) UVB. The cells were stained with an antibody to IL-10, 24 h after irradiation.
Results:
Preincubation with both selenium compounds inhibited UVB induction of IL-10 immunostaining, although selenomethionine was more effective. Pretreatment with 200 nmol L(-1) selenomethionine decreased IL-10 immunostaining to levels seen in the unirradiated controls.
Conclusions:
The protective effects of selenium against UVB-induced skin cancer in murine models may result, in part, from its ability to inhibit release of cytokines that are capable of suppressing cell-mediated immunity.