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We read with interest the article by Mehta and Martin¹ titled "A Case of Pemphigus Vulgaris Improved by Cigarette Smoking." We have a better explanation why cigarette smoking might be expected to improve skin lesions of patients with pemphigus vulgaris, particularly when nicotine in cigarette smoke contacts mucous membranes.

Human keratinocytes contain an elaborate acetylcholine network. Specifically, human keratinocytes synthesize, store, release, and degrade acetylcholine.² Keratinocytes contain choline acetyltransferase and acetylcholinesterase,² and have on their cell membranes both muscarinic and nicotinic receptors for acetylcholine.^3-4 Both nicotinic and muscarinic acetylcholine receptors regulate cell-to-cell adhesion of human keratinocytes (reviewed in Grando⁵). Interaction of nicotine (and other nicotinic agonists) with nicotinic acetylcholine receptors on keratinocytes opens ion gates in the cell membrane to help increase cell-to-cell adherence, stop acantholysis, and stimulate keratinocytes to move laterally to heal erosions.⁶

We believe the keratinocyte cholinergic system is altered in pemphigus.⁷ Keratinocytes undergoing acantholysis in . . . [Full Text of this Article]

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