Cytokine expression in trichloroethylene-induced hypersensitivity dermatitis: an in vivo and in vitro study.

The purpose of this study was to address the association between cytokine expression and the hypersensitivity dermatitis induced by trichloroethylene (TCE) exposure. 28 TCE-induced hypersensitivity dermatitis patients, 22 TCE exposed workers and 22 non-exposed controls were enrolled in the study. The serum levels of interleukin (IL)-1 beta, IL-6, IL-8 and tumor necrosis factor (TNF)-alpha were analyzed using a magnetic colorbead-based multiplex assay. The patients showed significantly higher levels of serum IL-1 beta (p = 0.033 and p = 0.015), IL-6 (p < 0.001), IL-8 (p < 0.001 and p = 0.002) and TNF-alpha (p = 0.009 and p = 0.005) than the TCE exposed workers and non-exposed controls. There was a significantly positive correlation among these cytokine concentrations, but no significant correlation was found between these cytokine concentrations and the disease duration in patient group. We further compared the effects of trichloroethanol (TCOH) and trichloroacetic acid (TCA), two major metabolites of TCE, on cytokine expression in keratinocyte cell line (HaCaT). IL-1 alpha, IL-6, IL-8 and TNF-alpha concentrations were tested using enzyme-linked immunosorbent assay (ELISA) after HaCaT cells were treated with different concentrations of TCOH or TCA for 24 h. We found that TCOH, but not TCA, increased the levels of IL-1 alpha and IL-6 in a dose-dependent manner. We also found that TCOH activated the nuclear factor kappa B (NF-kappa B) pathway. Bay 11-7082 (NF-kappa B inhibitor) significantly attenuated the TCOH-induced production of IL-6 in HaCaT cells, but IL-1 alpha production was not affected. In conclusions, it is suggested that IL-1 beta, IL-6, IL-8 and TNF-alpha were associated with TCE-induced hypersensitivity dermatitis. TCOH induced IL-6 expression through activation of the NF-kappa B pathway in HaCaT cells and may play an integral role in TCE-induced skin hypersensitivity. (C) 2012 Elsevier Ireland Ltd. All rights reserved.