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.
KeywordsStratum Corneum Platelet Activate Factor Psoriatic Skin Systemic Mastocytosis Chronic Plaque Psoriasis
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- 4.S. Hammarstrom, M. Hamberg, B. Samuelsson, E.A. Duell, M. Stawiski and J.J. Voorhees, Increased concentrations of non-esterified arachidonic acid, 12L-hydroxyeicosatetraenoic acid, Prostaglandin E2 and Prostaglandin F2 α in the epidermis of psoriasis, Proc. Natl. Acad. Sci. 72:5130 (1975).PubMedCrossRefGoogle Scholar
- 8.N. Fincham, R. Camp and I. Leigh, Synthesis of arachidonate lipoxygenase products by epidermal cells, J. Invest. Dermatol. 84:447 (1985).Google Scholar
- 9.J. Grabbe, T. Rosenbach and B. Czarnetzki, Production of LTB4-like chemotactic arachidonate metabolites from human keratinocytes, J. Invest. Dermatol. 85:527.Google Scholar
- 15.P.M. Woollard, G.M. Murphy, F.M. Cunningham, R.D.R. Camp and M.W. Greaves, Proinflammatory effects of 12(R)-hydroxy-5,8,10,14 eicosatetraenoic acid in human skin, Br. J. Dermatol. 118:277 (1988).Google Scholar
- 21.R. Camp, A. Kobza Black, F. Cunningham, A. Mallet and M. Greaves, Pharmacological effects of topical lonapalene in psoriasis, J. Invest. Dermatol. 90:550 (1988).Google Scholar
- 28.R.D.R. Camp and F.M. Cunningham, The role of eicosanoids in inflammatory disorders of the skin, in: “Advances in Eicosanoid Research: Eicosanoids in inflammatory conditions of the lung, skin and joints” M. Church and C. Robinson ed., MTP Press, Lancaster/Boston/The Hague/Dordrecht (1988).Google Scholar
- 39.E. Henocq and B.B. Vargaftig, Skin eosinophilia in atopic patients, J. Allergy clin. Immunol. 79:248 (1987).Google Scholar
- 40.F. Valone, M. Shalit, P. Atkins, E. Goetzl and B. Sireiman, Platelet activating factor release in allergic skin sites in humans, J. Allergy clin. Immunol. 79:248 (1987).Google Scholar
- 45.A.I. Mallet, F.M. Cunningham, E. Wong and M.W. Greaves, Platelet activating factor in chronic plaque psoriasis in: “Adv. in Prostaglandin, Thromboxane and Leukotriene Res. Vol. 17” B. Samuelsson, R. Paoletti and P. Ramwell, eds. Raven Press, New York (1987).Google Scholar
- 47.F.M. Cunningham, I. Leigh and A.I. Mallet, The production of platelet activating factor (PAF) by human epidermal cells, Br. J. Pharmacol. 91:117P (1987).Google Scholar
- 49.P. Braquet, L. Touqui, T.Y. Shen and B.B. Vargaftig, Perspectives in platelet activating factor research, Pharmacol. Revs. 39:97 (1987).Google Scholar
- 60.N.J. Fincham, R.D.R. Camp, A.J.H. Gearing, C.R. Bird and F.M. Cunningham, Neutrophil chemoattractant and IL-1-like activity in samples from psoriatic skin lesions, J. Immunol. 140:294 (1988).Google Scholar