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dc.contributor.authorGreene, Catherine M
dc.contributor.authorRamsay, Hugh
dc.contributor.authorWells, Robert J
dc.contributor.authorO'Neill, Shane J
dc.contributor.authorMcElvaney, Noel G
dc.date.accessioned2010-07-15T12:38:46Z
dc.date.available2010-07-15T12:38:46Z
dc.date.issued2010
dc.identifier.citationInhibition 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.issn1466-1861
dc.identifier.pmid20379354
dc.identifier.doi10.1155/2010/423241
dc.identifier.urihttp://hdl.handle.net/10147/107720
dc.description.abstractCystic 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.isoenen
dc.subject.meshCell Line
dc.subject.meshCell Proliferation
dc.subject.meshCystic Fibrosis
dc.subject.meshEpithelial Cells
dc.subject.meshHumans
dc.subject.meshInterleukin-8
dc.subject.meshLaser Scanning Cytometry
dc.subject.meshLipopolysaccharides
dc.subject.meshNicotine
dc.subject.meshPeptidoglycan
dc.subject.meshReceptors, Nicotinic
dc.subject.meshToll-Like Receptor 2
dc.subject.meshToll-Like Receptor 4
dc.subject.meshTrachea
dc.subject.meshZymosan
dc.titleInhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor.en
dc.contributor.departmentDepartment of Medicine, RCSI Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. cmgreene@rcsi.ieen
dc.identifier.journalMediators of inflammationen
refterms.dateFOA2018-08-22T08:33:06Z
html.description.abstractCystic 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.


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