Azithromycin attenuates effects of lipopolysaccharide on lung allograft bronchial epithelial cells

  1. Lookup NU author(s)
  2. Adillah Binti Yusof
  3. Dr Ian Forrest
  4. Professor Paul Corris
  5. Therese Small
  6. Debra Jones
  7. Professor Andrew Fisher
  8. Professor Tim Cawston
  9. Dr James Lordan
  10. Dr Christopher Ward
Author(s)Murphy DM, Forrest IA, Corris PA, Johnson GE, Small T, Jones D, Fisher AJ, Egan JJ, Cawston TE, Lordan JL, Ward C
Publication type Article
JournalThe Journal of Heart and Lung Transplantation
Year2008
Volume27
Issue11
Pages1210-6
ISSN (print)1053-2498
ISSN (electronic)1557-3117
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BackgroundThe bronchial epithelium is a source of mediators that may play a role in the airway inflammation and remodeling of post-transplant obliterative bronchiolitis (OB). Traditional strategies have failed to have an impact on OB. Recent studies have suggested a role for azithromycin in managing the condition. In this study we aimed to determine the effect of azithromycin on LPS-mediated epithelial release of factors relevant to airway neutrophilia and remodeling in a unique population of primary bronchial epithelial cells (PBECs) derived from stable lung allografts. MethodsPBECs were established from bronchial brushings of stable lung transplant recipients and treated with lipopolysaccharide (LPS, 0.1, 1 and 10 μg/ml) for 48 hours. Interleukin-8 (IL-8), granulocyte macrophage colony-stimulating factor (GM-CSF) and vascular endothelial growth factor (VEGF) protein levels were measured by Luminex analyzer. PBECs were then incubated with LPS and azithromycin, and protein levels were again determined. ResultsLPS caused a significant increase in IL-8 and GM-CSF at concentrations of 1 and 10 μg/ml, with no effect on VEGF release. Azithromycin caused a significant decrease in the LPS-stimulated IL-8 and GM-CSF release. ConclusionsLPS upregulates release of IL-8 and GM-CSF from PBECs derived from stable lung allografts. Sub-microbicidal concentrations of azithromycin attenuate this and may, therefore, alleviate infection-driven neutrophilic airway inflammation and remodeling in the allograft airway.
PublisherElsevier Inc.
URLhttp://dx.doi.org/10.1016/j.healun.2008.07.026
DOI10.1016/j.healun.2008.07.026
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