Raised interleukin-17 is immunolocalised to neutrophils in cystic fibrosis lung disease

  1. Lookup NU author(s)
  2. Dr Malcolm Brodlie
  3. Dr Michael McKean
  4. Dr Amy Anderson
  5. Dr Catharien Hilkens
  6. Professor Andrew Fisher
  7. Professor Paul Corris
  8. Dr James Lordan
  9. Dr Christopher Ward
Author(s)Brodlie M, McKean MC, Johnson GE, Anderson AE, Hilkens CM, Fisher AJ, Corris PA, Lordan JL, Ward C
Publication type Article
JournalEuropean Respiratory Journal
ISSN (print)0903-1936
ISSN (electronic)1399-3003
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Abstract Interleukin-17 is pivotal in orchestrating the activity of neutrophils. Neutrophilic inflammation is the dominant pathology in cystic fibrosis lung disease. We investigated interleukin-17 protein expression in the lower airway in cystic fibrosis, its cellular immuno-localisation and the effects of interleukin-17 on cystic fibrosis primary bronchial epithelial cells. Immunohistochemistry was performed on explanted cystic fibrosis lungs and compared to the non-suppurative condition pulmonary hypertension. Airway lavages and epithelial cultures were generated from explanted cystic fibrosis lungs. Immunoreactivity for interleukin-17 was significantly increased in the lower airway epithelium in cystic fibrosis (median 14.1%) compared to pulmonary hypertension (2.95%, P=0.0001). The number of cells staining positive for interleukin-17 in the lower airway mucosa was also increased (64 compared to 9/mm basement membrane, P=0.0005) and included both neutrophils in addition to mononuclear cells. Interleukin-17 was detectable in airway lavages from explanted cystic fibrosis lungs. Treatment of epithelial cultures with interleukin-17 increased production of interleukin-8, interleukin-6 and granulocyte macrophage colony-stimulating factor. In conclusion, immunoreactive interleukin-17 is raised in the lower airway of people with cystic fibrosis and localises to both neutrophils and mononuclear cells. Interleukin-17 increases production of pro-neutrophilic mediators by cystic fibrosis epithelial cells, suggesting potential for a positive feedback element in airway inflammation.
PublisherEuropean Respiratory Society
PubMed id21109552
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