PubMed · 6784653
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E Grosshans, M Henry, G Tell, P J Schechter, P Böhlen, J Grove, J Koch-Weser. 1980. [Polyamines in psoriasis].. https://pubmed.ncbi.nlm.nih.gov/6784653/
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Anthralin is among the most effective agents for the topical treatment of psoriasis. However, this drug causes unpleasant side-effects such as inflammation and staining of the nonaffected skin surrounding a psoriatic lesion. The biochemical basis for the induction of an inflammatory response in the skin and the antipsoriatic effectiveness are uncertain, although several cellular targets of anthralin action have been identified. Because no single mechanism is operative, the view was taken that all the effects exerted by anthralin are caused by its redox activity leading to the generation of anthralin free radicals and oxygen radicals. Clear relationships between oxygen-radical production by anthralin and biological response are evident with respect to chemical lesions in cellular macromolecules such as DNA, lipid membranes, and enzymes, indicating that these species account for the antipsoriatic and proinflammatory effects elicited by anthralin. This poses new challenges for the medicinal chemist and provides impetus for identifying novel compounds having potential for an improved therapeutic index.
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Atopic dermatitis is a lymphocyte-mediated skin disease. We studied the expression of the adhesion molecule alpha6 integrin by immunohistochemistry in spontaneous atopic inflammation as well as during the eliciting phase of atopen (Dermatophagoides pteronyssinus), antigen (nickel sulfate) and irritative (anthralin) induced patch test reactions in atopic skin. Results were compared with nickel sulfate patch test reactions in normal skin. A role of the alpha6 integrin, expressed at the luminal side of blood vessels, for T cell migration in lesional atopic skin was supposed. In normal human skin the alpha6 integrin was weakly expressed by blood vessels and by basal epithelial cells of the epidermis. In acute and chronic lesional skin of patients with atopic dermatitis dramatic upregulation of alpha6 integrin expression was observed on endothelial cells and in the epidermis. The similar pattern of upregulated suprabasal alpha6 integrin expression was established in the patch test reactions 48 h after atopen and antigen application or irritation of the skin without differences in dependence on the eliciting substance. No difference of alpha6 integrin expression was seen between atopic and normal skin. Tumor necrosis factor alpha, interleukin-1, interleukin-4 and interferon gamma play a role in atopic inflammation. Tumor growth factor beta and interleukin-6 are mitogenic/growth factors for keratinocytes. For this reason the effect of these cytokines and of phorbol-12-myristate-13-acetate on the expression level of alpha6 integrin was tested in short-term skin organ culture of normal and atopic skin as well as in keratinocyte cultures. In these assays no cytokines had an effect on alpha6 integrin expression suggesting another mechanism which regulates this integrin. However, the increased expression of alpha6 integrin in the suprabasal epidermis is associated with a T cell influx into the epidermis. We speculate that the alpha6 integrin expression may lead to an epidermotropism of T cells during inflammation.