期刊
BRITISH JOURNAL OF DERMATOLOGY
卷 146, 期 3, 页码 383-391出版社
WILEY
DOI: 10.1046/j.1365-2133.2002.04640.x
关键词
nicotine; nicotinic acetylcholine receptors; non-smokers; palmoplantar pustulosis; smokers
类别
Background A suggested role for nicotine in the pathogenesis of palmoplantar pustulosis (PPP) has been discussed. The target for the inflammation in PPP is the acrosyringium. Nicotine acts as an agonist on nicotinic acetylcholine receptors (nAChRs) and can influence a variety of cellular functions. Objectives To study the alpha3- and alpha7-nAChR expression in palmar skin of patients with PPP in comparison with that in healthy smoking and non-smoking controls. Methods Biopsies from 20 patients with PPP, seven healthy smokers and eight healthy non-smokers were studied by immunohistochemistry with a monoclonal anti-alpha3 and a polyclonal anti-alpha7 antibody. Results In healthy controls both nAChR subtypes showed stronger immunoreactivity in the eccrine glands and ducts than in the epidermis. The papillary endothelium was positive for both subtypes. Epidermal alpha3 staining was stronger and that of the coil and dermal ducts weaker in healthy smokers than in healthy non-smokers. In involved PPP skin, granulocytes displayed strong alpha3 immunoreactivity. The normal epidermal alpha7 staining pattern was abolished in PPP skin and was replaced by strong mesh-like surface staining, most markedly adjacent to the acrosyringium, which in controls was intensely alpha7 positive at this level. Endothelial alpha7 staining was stronger in PPP skin than in the controls. Conclusions Smoking can influence nAChR expression. The altered nAChR staining pattern in PPP skin may indicate a possible role for nicotine in the pathogenesis of PPP. We hypothesize that there is an abnormal response to nicotine in patients with PPP, resulting in inflammation.
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