Dermatology research: contact dermatitis
Margarida Gonçalo (HUC), Américo Figueiredo (HUC), Teresa Cruz (CNC), Celeste Lopes (CNC)
As part of the collaboration with the Department of Dermatology of the University Hospital, we have two main objectives: the identification of new therapeutic targets for allergic contact dermatitis and the identification of cellular markers that allow the in vitro recognition of the skin sensitization potential of environmental chemicals. Our results show that among all the chemicals studied, namely the contact sensitizers (2,4-dinitrofluorbenzene (DNFB), 1,4-phenylenediamine (PPD), nickel sulphate (NiSO4)), the inactive analogue of DNFB, 2,4-dichloronitrobenzene (DCNB) and two irritants (sodium dodecyl sulphate and benzalkonium chloride), only NiSO4 increased the expression of inducible nitric oxide synthase (iNOS) in skin dendritic cells. We compared the effects of three different immunosuppressors on the iNOS expression and NO production elicited by the contact sensitizer NiSO4. The results show that dexamethasone, unlike cyclosporin A and sirolimus, inhibited iNOS expression and NO production stimulated by the contact sensitizer nickel sulphate. This can explain, at least in part, why topical and systemic steroids are more effective in the treatment of allergic contact dermatitis than the new immunosuppressors. More recently, we found that the skin sensitizers, DNFB, PPD and NiSO4, modulate the expression of dendritic cell surface molecules (chemokine and cytokine receptors), the cytokines production and transcription factors activation differently from skin irritants.
PUBLICATIONS
Cruz M.T., Gonçalo M., Figueiredo A., Duarte C.B. and Lopes M.C. Effect of skin sensitizers on inducible nitric oxide synthase expression and nitric oxide production in skin dendritic cells: role of different immunosuppressive drugs. Immunopharmacology and Immunotoxicology (in press).
Gonçalo M., Cruz M.T., Duarte C.B., Figueiredo A., Lopes M.C. (2006). Immunossupressive Drugs in Ni-induced iNOS expression in skin dendritic cells. Contact Dermatitis, 55 S1: 43
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