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Restoring Bacterial Killing In Cystic Fibrosis

  December, 13 2007 10:30
your information resource in human molecular genetics

A report online in Nature Medicine reveals that high protease levels in the lungs of patients with cystic fibrosis disable immune cells, explaining why CF patients fail to clear lung infections. The findings also offer a therapeutic strategy to boost bacterial killing in these patients.

Individuals with cystic fibrosis have high levels of the protein IL-8 in their lungs. IL-8 normally triggers bacterial killing by immune cells called neutrophils, but the lungs of CF patients are often colonized by bacteria, despite the presence of high numbers of lung neutrophils. Somehow, the neutrophils of CF patients do not function properly.

Dominik Hartl and colleagues report that IL-8 activates neutrophils by binding to a cytokine receptor termed CXCR1. CF patients have abnormally high levels of lung proteases, as well as high levels of the neutrophil-activating cytokine IL-8. This high protease activity explains both the defective neutrophil function and the high levels of IL-8 in the lungs of CF patients. The proteases cleave the CXCR1 receptor, effectively disabling the neutrophils' bacterial killing activity by making the cells unresponsive to IL-8. Meanwhile, the cleaved receptor fragment stimulates further secretion of IL-8 from lung epithelial cells by interacting with the protein toll-like receptor 2.

The authors also found that CF patients receiving four weeks of inhalation therapy with alpha1-antitrypsin -- a protease inhibitor -- have reduced numbers of the bacteria Pseudomonas aeruginosa in their sputum, which correlates with improvements in the bacterial killing ability of neutrophils, restoration of CXCR1 on the surface of the neutrophils and reduced amounts of the soluble receptor fragment in the lungs of the CF patients.

Author contact:

Dominik Hartl (Children's Hospital, Munich, Germany)
E-mail: dominic.hartl@med.uni-muenchen.de

Abstract available online.

(C) Nature Medicine press release.

Message posted by: Trevor M. D'Souza

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