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    IL-8 dictates glycosaminoglycan binding and stability of IL-18 in cystic fibrosis.

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    Authors
    Reeves, Emer P
    Williamson, Michael
    Byrne, Barry
    Bergin, David A
    Smith, Stephen G J
    Greally, Peter
    O'Kennedy, Richard
    O'Neill, Shane J
    McElvaney, Noel G
    Affiliation
    Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin, Ireland. emerreeves@rcsi.ie
    Issue Date
    2010-02-01
    MeSH
    Adolescent
    Binding, Competitive
    Bronchoalveolar Lavage Fluid
    Cell Line, Transformed
    Child
    Child, Preschool
    Cystic Fibrosis
    Down-Regulation
    Glycosaminoglycans
    Humans
    Inflammation Mediators
    Interleukin-18
    Interleukin-8
    Jurkat Cells
    Protein Binding
    Protein Stability
    Up-Regulation
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    Citation
    IL-8 dictates glycosaminoglycan binding and stability of IL-18 in cystic fibrosis. 2010, 184 (3):1642-52 J. Immunol.
    Journal
    Journal of immunology (Baltimore, Md. : 1950)
    URI
    http://hdl.handle.net/10147/127096
    DOI
    10.4049/jimmunol.0902605
    PubMed ID
    20026745
    Additional Links
    http://www.jimmunol.org/content/184/3/1642.full.pdf+html
    Abstract
    Dysregulation of airway inflammation contributes to lung disease in cystic fibrosis (CF). Inflammation is mediated by inflammatory cytokines, including IL-8, which illustrates an increase in biological half-life and proinflammatory activity when bound to glycosaminoglycans (GAGs). The aim of this project was to compare IL-8 and IL-18 for their relative stability, activity, and interaction with GAGs, including chondroitin sulfate, hyaluronic acid, and heparan sulfate, present in high quantities in the lungs of patients with CF. Bronchoalveolar lavage fluid was collected from patients with CF (n = 28), non-CF controls (n = 14), and patients with chronic obstructive pulmonary disease (n = 12). Increased levels of IL-8 and reduced concentrations of IL-18 were detected in bronchial samples obtained from CF individuals. The low level of IL-18 was not a defect in IL-18 production, as the pro- and mature forms of the molecule were expressed and produced by CF epithelial cells and monocytes. There was, however, a marked competition between IL-8 and IL-18 for binding to GAGs. A pronounced loss of IL-18 binding capacity occurred in the presence of IL-8, which displaced IL-18 from these anionic-matrices, rendering the cytokine susceptible to proteolytic degradation by neutrophil elastase. As a biological consequence of IL-18 degradation, reduced levels of IL-2 were secreted by Jurkat T lymphocytes. In conclusion, a novel mechanism has been identified highlighting the potential of IL-8 to determine the fate of other inflammatory molecules, such as IL-18, within the inflammatory milieu of the CF lung.
    Item Type
    Article
    Language
    en
    ISSN
    1550-6606
    ae974a485f413a2113503eed53cd6c53
    10.4049/jimmunol.0902605
    Scopus Count
    Collections
    Beaumont Hospital

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