Patients with guttate psoriasis have been reported to respond to anticholinergic treatment. We wanted to know how the cholinergic system could be involved in this process. Mast cells are characteristic components of the inflammatory infiltrate of guttate psoriasis. We therefore studied the cholinergic system in both epidermis and mast cells of 10 patients with guttate psoriasis in involved and uninvolved skin on protein level using immunofluorescence and in a mast cell line (HMC-1) using PCR. Both in vivo and in vitro, mast cells lacked expression of cholinacetyl transferase, vesicular acetylcholine transporter and choline transporter-1 but contained high levels of acetylcholinesterase and different nicotinic and muscarinic acetylcholine receptor (AChR). In lesional epidermis, both acetylcholine production and AChR expression was mostly shifted from the basal to the suprabasal layers. In vitro, acetylcholine, choline and nicotine, but not muscarine, induced mast cell degranulation but not LTB-4 or TNF-alpha secretion. This process could be inhibited by low doses of different nicotinic acetylcholine receptor antagonists.
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