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Exploitation of the nicotinic anti-inflammatory pathway for the treatment of epithelial inflammatory diseases.

Abstract
Discoveries in the first few years of the 21st century have led to an understanding of important interactions between the nervous system and the inflammatory response at the molecular level, most notably the acetylcholine (ACh)-triggered, alpha7-nicotinic acetylcholine receptor (alpha7nAChR)-dependent nicotinic anti-inflammatory pathway. Studies using the alpha7nAChR agonist, nicotine, for the treatment of mucosal inflammation have been undertaken but the efficacy of nicotine as a treatment for inflammatory bowel diseases remains debatable. Further understanding of the nicotinic anti-inflammatory pathway and other endogenous anti-inflammatory mechanisms is required in order to develop refined and specific therapeutic strategies for the treatment of a number of inflammatory diseases and conditions, including periodontitis, psoriasis, sarcoidosis, and ulcerative colitis.
AuthorsDavid A Scott, Michael Martin
JournalWorld journal of gastroenterology (World J Gastroenterol) Vol. 12 Issue 46 Pg. 7451-9 (Dec 14 2006) ISSN: 1007-9327 [Print] United States
PMID17167832 (Publication Type: Journal Article, Review)
Chemical References
  • Nicotinic Agonists
  • Receptors, Nicotinic
  • Nicotine
Topics
  • Humans
  • In Vitro Techniques
  • Inflammation (drug therapy, physiopathology)
  • Inflammatory Bowel Diseases (drug therapy, physiopathology)
  • Models, Biological
  • Nicotine (pharmacology)
  • Nicotinic Agonists (pharmacology)
  • Periodontitis (drug therapy, physiopathology)
  • Psoriasis (drug therapy, physiopathology)
  • Receptors, Nicotinic (drug effects, physiology)
  • Sarcoidosis (drug therapy, physiopathology)

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