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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.

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    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
    Issue Date
    2010
    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
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    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
    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
    ISSN
    1466-1861
    ae974a485f413a2113503eed53cd6c53
    10.1155/2010/423241
    Scopus Count
    Collections
    Journal articles & published research

    entitlement

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