• nicotine;
  • nicotinic acetylcholine receptors;
  • non-smokers;
  • palmoplantar pustulosis;
  • smokers

SummaryBackground 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 α3- and α7-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-α3 and a polyclonal anti-α7 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 α3 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 α3 immunoreactivity. The normal epidermal α7 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 α7 positive at this level. Endothelial α7 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.