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The potential role of acetylcholine receptors in acne inversa (HS) pathogenesis
Author(s) -
Kurzen Hjalmar,
Hana Anisa,
Frongia Giovanni,
Goerdt Sergij,
Gratchev Alexei
Publication year - 2006
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2006.0436i.x
Subject(s) - nicotinic agonist , choline acetyltransferase , acetylcholine receptor , cholinergic , acetylcholine , epidermis (zoology) , muscarinic acetylcholine receptor , nicotine , hair follicle , receptor , chemistry , endocrinology , biology , microbiology and biotechnology , medicine , anatomy
Acne inversa is a chronic inflammatory disorder that has been shown to be influenced by tobacco smoking, which may represent a ‘natural’ model of exogenous nicotine‐mediated activation of the nicotinic acetylcholine receptors (AChR). In previous works, we have provided a concise mapping of AChR present in normal skin and have demonstrated a crucial role of AChR in terminal differentiation and barrier formation. In addition, several studies suggest a role for the non‐neuronal cholinergic system in immunomodulation. To date, the AChR composition of the cells involved in the pathogenesis of acne inversa has not yet been characterized. Using immunohistochemistry and RT – PCR, we could show that nicotinic α3, α5, α7 and α9 AChR as well as muscarinic M 1 –M 5 AChR are produced in lesional epidermis in a pattern comparable with normal epidermis. In vitro and in lesional skin, we could demonstrate the presence of α3, α5 and α7 nAChR as well as M 1 –M 5 mAChR in variable amounts on macrophages. In lesional epidermis, the choline‐acetyltransferase (ChAT)‐reactivity was particularly pronounced in the epidermal basal layer, while in the sinus tracts, ChAT reactivity was extended to all epithelial layers. High levels of ChAT especially in the hair follicle infundibulum indicate that endogenously produced ACh may act synergistically with tobacco‐delivered nicotine in aggravating infundibular hyperkeratosis. ChAT could not be detected in macrophages in vitro or in vivo indicating that macrophages do not actively contribute to ACh signalling in acne inversa but may rather be targets of ACh, and hence nicotine induced immunomodulation.