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    Hypoxia and sterile inflammation in cystic fibrosis airways: Mechanisms and potential therapies

    Access Status
    Fulltext not available
    Authors
    Montgomery, S.T.
    Mall, M.A.
    Kicic, Anthony
    Stick, S.M.
    Date
    2017
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Montgomery, S.T. and Mall, M.A. and Kicic, A. and Stick, S.M. 2017. Hypoxia and sterile inflammation in cystic fibrosis airways: Mechanisms and potential therapies. European Respiratory Journal. 49 (1): UNSP 1600903.
    Source Title
    European Respiratory Journal
    DOI
    10.1183/13993003.00903-2016
    ISSN
    0903-1936
    Faculty
    Faculty of Health Sciences
    School
    School of Public Health
    URI
    http://hdl.handle.net/20.500.11937/76811
    Collection
    • Curtin Research Publications
    Abstract

    Copyright © ERS 2017. Cystic fibrosis is one of the most common autosomal recessive genetic diseases in Caucasian populations. Diagnosis via newborn screening and targeted nutritional and antibiotic therapy have improved outcomes, however respiratory failure remains the key cause of morbidity and mortality. Progressive respiratory disease in cystic fibrosis is characterised by chronic neutrophilic airway inflammation associated with structural airway damage leading to bronchiectasis and decreased lung function. Mucus obstruction is a characteristic early abnormality in the cystic fibrosis airway, associated with neutrophilic inflammation often in the absence of detectable infection. Recent studies have suggested a link between hypoxic cell death and sterile neutrophilic inflammation in cystic fibrosis and other diseases via the IL-1 signalling pathway. In this review, we consider recent evidence regarding the cellular responses to respiratory hypoxia as a potential driver of sterile neutrophilic inflammation in the lung, current knowledge on hypoxia as a pathogenic mechanism in cystic fibrosis and the potential for current and future therapies to alleviate hypoxia-driven sterile inflammation.

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