Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor.

Hdl Handle:
http://hdl.handle.net/10147/107720
Title:
Inhibition of Toll-like receptor 2-mediated interleukin-8 production in Cystic Fibrosis airway epithelial cells via the alpha7-nicotinic acetylcholine receptor.
Authors:
Greene, Catherine M; Ramsay, Hugh; Wells, Robert J; O'Neill, Shane J; McElvaney, Noel G
Affiliation:
Department of Medicine, RCSI Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland. cmgreene@rcsi.ie
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.
Journal:
Mediators of inflammation
Issue Date:
2010
URI:
http://hdl.handle.net/10147/107720
DOI:
10.1155/2010/423241
PubMed ID:
20379354
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.
Language:
en
MeSH:
Cell Line; Cell 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
ISSN:
1466-1861

Full metadata record

DC FieldValue Language
dc.contributor.authorGreene, Catherine Men
dc.contributor.authorRamsay, Hughen
dc.contributor.authorWells, Robert Jen
dc.contributor.authorO'Neill, Shane Jen
dc.contributor.authorMcElvaney, Noel Gen
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

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