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Adherence of airway neutrophils and inflammatory response are increased in CF airway epithelial cell-neutrophil

Olivier Tabary1, Harriet Corvol, Emilie Boncoeur

  • 1Inserm U719, Hôpital St-Antoine, Bâtiment Kourilsky, 184, rue du Fg St-Antoine, F-75571 Paris, France.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|November 8, 2005
PubMed

Insights

In cystic fibrosis (CF) airways, more neutrophils (PMN) adhere to lung cells, increasing inflammation. Blocking adhesion molecules reduces this effect, suggesting a target for CF treatments.

Area of Science:

  • Immunology
  • Pulmonology
  • Cell Biology

Background:

  • Persistent neutrophil presence in airways is characteristic of cystic fibrosis (CF).
  • Understanding neutrophil behavior and inflammatory mediator production in CF airways is crucial.

Purpose of the Study:

  • To assess neutrophil (PMN) adherence, apoptosis, and IL-6/IL-8 production in airway epithelial cells from CF patients.
  • To investigate the role of CFTR mutations in PMN-epithelial cell interactions and subsequent inflammation.

Main Methods:

  • Coculture of neutrophils from CF and non-CF individuals with bronchial epithelial cells (CFTR-mutated vs. corrected).
  • Quantification of PMN adherence, apoptosis rates, and IL-6/IL-8 levels.
  • Inhibition of adhesion molecules (ICAM-1, VCAM-1, E-selectin) using monoclonal antibodies (MAbs).

Main Results:

  • CF neutrophils exhibited significantly higher adherence to CFTR-deficient epithelial cells compared to non-CF neutrophils on corrected cells.
  • IL-6 and IL-8 levels were markedly elevated in cocultures involving CF neutrophils and CFTR-deficient cells.
  • Blocking ICAM-1, VCAM-1, and E-selectin reduced CF PMN adherence by 50-64%.

Conclusions:

  • Increased adherence of non-apoptotic neutrophils to airway epithelium in CF, coupled with elevated IL-6/IL-8, likely drives sustained airway inflammation.
  • Targeting adhesion molecules may offer a therapeutic strategy to mitigate exaggerated inflammatory responses in CF airways.

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