Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor.
Affiliation
Department of Medicine, RCSI Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. cmgreene@rcsi.ieIssue Date
2010MeSH
Cell LineCell Proliferation
Cystic Fibrosis
Epithelial Cells
Humans
Interleukin-8
Laser Scanning Cytometry
Lipopolysaccharides
Nicotine
Peptidoglycan
Receptors, Nicotinic
Toll-Like Receptor 2
Toll-Like Receptor 4
Trachea
Zymosan
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Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor. 2010, 2010:423241 Mediators Inflamm.Journal
Mediators of inflammationDOI
10.1155/2010/423241PubMed ID
20379354Abstract
Cystic Fibrosis (CF) is an inherited disorder characterised by chronic inflammation of the airways. The lung manifestations of CF include colonization with Pseudomonas aeruginosa and Staphylococcus aureus leading to neutrophil-dominated airway inflammation and tissue damage. Inflammation in the CF lung is initiated by microbial components which activate the innate immune response via Toll-like receptors (TLRs), increasing airway epithelial cell production of proinflammatory mediators such as the neutrophil chemokine interleukin-8 (IL-8). Thus modulation of TLR function represents a therapeutic approach for CF. Nicotine is a naturally occurring plant alkaloid. Although it is negatively associated with cigarette smoking and cardiovascular damage, nicotine also has anti-inflammatory properties. Here we investigate the inhibitory capacity of nicotine against TLR2- and TLR4-induced IL-8 production by CFTE29o- airway epithelial cells, determine the role of alpha7-nAChR (nicotinic acetylcholine receptor) in these events, and provide data to support the potential use of safe nicotine analogues as anti-inflammatories for CF.Language
enISSN
1466-1861ae974a485f413a2113503eed53cd6c53
10.1155/2010/423241
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