Pro-Inflammatory Mediators and Human Skin Disease
Human skin diseases are many and diverse in nature, ranging from conditions where the primary abnormality is a transient disorder of the vasculature, one example being urticaria, to conditions such as psoriasis, which are characterised by a chronic cellular infiltrate. It has been suggested that the pathological changes associated with these skin diseases may be brought about by chemical mediators present in the involved tissue. Before any aspect of disease pathology is ascribed to the actions of a particular compound, however, certain criteria must first be satisfied. The mediator, should be identified in lesional tissue and, ideally, the absolute amounts compared to those in clinically normal skin. If other compounds with similar modes of actions are also present it is useful to ascertain the relative amounts of each since, although one mediator may be considerably less potent in eliciting a particular response, the difference in potency may be rendered of little importance if that compound is present in correspondingly greater amounts in vivo. The ability of cells derived from the skin to produce the mediator in vitro following stimulation suggests that release from the resident skin cell population may contribute to the endogenous levels measured, although whether such release is a primary event in the evolution of a lesion, or occurs secondarily in response to tissue damage cannot readily be determined.
KeywordsHigh Performance Liquid Chromatography Nicotinate Histamine Prostaglandin Vasculitis
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