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Nickel-induced cytokine production from mononuclear cells in nickel sensitive individuals and controls.

Tidsskriftartikel - 2000

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Exposure to nickel is a major cause of allergic contact dermatitis which is considered to be an inflammatory response induced by antigen-specific T cells. Here we describe the in vitro analysis of the nickel-specific T-cell-derived cytokine response of peripheral blood mononuclear cells from 35 nickel-allergic and 30 non-nickel-allergic individuals. Peripheral blood mononuclear cells were stimulated with 10-4 and 10-5 mol/l NiSO4 for 6 days and then additionally with ionomycin and phorbol myristate acetate for 24 h. Culture supernatants were analysed for interleukin-4 (IL-4), IL-5, interferon-% (IFN-%) and tumour necrosis factor-! (TNF-!) by quantitative ELISA. The analysis showed that the synthesis of IL-4 and IL-5 but not of IFN-% or TNF-! was significantly higher in the nickel-allergic individuals. The finding of preferential synthesis of Th2 cytokines was somewhat of a surprise, since previous studies have suggested a Th1 response in nickel-mediated allergic contact dermatitis. Subsequently, the nickel-allergic individuals were randomized to experimental exposure to nickel or vehicle in a double-blind design. A daily 10-min exposure of one finger to 10 ppm nickel solution for 1 week followed by 100 ppm for an additional week evoked a clinical response of hand eczema in the nickel-exposed group. Blood samples were drawn on days 7 and 14 after the start of this exposure to occupationally relevant concentrations of nickel. No statistically significant differences were observed in the nickel-induced in vitro cytokine response during the exposure period. Our results indicate the possibility that IL-4 and IL-5 are involved in the pathogenesis of nickel-mediated contact dermatitis.

Reference

Borg L, Christensen J, Kristiansen J, Nielsen N, Menné T, Poulsen L. Nickel-induced cytokine production from mononuclear cells in nickel sensitive individuals and controls.. Arch Dermatol Res 2000;292(6):285-291.
doi: 10.1007/s004030000129

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