Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor.
dc.contributor.author | Greene, Catherine M | |
dc.contributor.author | Ramsay, Hugh | |
dc.contributor.author | Wells, Robert J | |
dc.contributor.author | O'Neill, Shane J | |
dc.contributor.author | McElvaney, Noel G | |
dc.date.accessioned | 2010-07-15T12:38:46Z | |
dc.date.available | 2010-07-15T12:38:46Z | |
dc.date.issued | 2010 | |
dc.identifier.citation | 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. | en |
dc.identifier.issn | 1466-1861 | |
dc.identifier.pmid | 20379354 | |
dc.identifier.doi | 10.1155/2010/423241 | |
dc.identifier.uri | http://hdl.handle.net/10147/107720 | |
dc.description.abstract | 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. | |
dc.language.iso | en | en |
dc.subject.mesh | Cell Line | |
dc.subject.mesh | Cell Proliferation | |
dc.subject.mesh | Cystic Fibrosis | |
dc.subject.mesh | Epithelial Cells | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Interleukin-8 | |
dc.subject.mesh | Laser Scanning Cytometry | |
dc.subject.mesh | Lipopolysaccharides | |
dc.subject.mesh | Nicotine | |
dc.subject.mesh | Peptidoglycan | |
dc.subject.mesh | Receptors, Nicotinic | |
dc.subject.mesh | Toll-Like Receptor 2 | |
dc.subject.mesh | Toll-Like Receptor 4 | |
dc.subject.mesh | Trachea | |
dc.subject.mesh | Zymosan | |
dc.title | Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor. | en |
dc.contributor.department | Department of Medicine, RCSI Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. cmgreene@rcsi.ie | en |
dc.identifier.journal | Mediators of inflammation | en |
refterms.dateFOA | 2018-08-22T08:33:06Z | |
html.description.abstract | 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. |