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Cleavage of CXCR1 on neutrophils disables bacterial killing in cystic fibrosis lung disease
Interleukin-8 (IL-8) activates neutrophils via the chemokine receptors CXCR1 and CXCR2. According to a recent study by Dominik Hartl from the Ludwig-Maximilian University in Munich, IL-8 enhances the killing of bacteria by neutrophils through CXCR1, but not CXCR2.
Cystic fibrosis leads frequently to colonisation of the airway by bacterial pathogens, although great numbers of neutrophils and IL-8 are present. Proteolytic activity in the airways of such individuals remained high, CXCR1 on neutrophils was cleaved and their bactericidal ability deactivated. These complications were protease concentration-dependent and also arose - less severe - in patients with chronic obstructive pulmonary disease.
Cleaving the receptor resulted in the release of glycosylated CXCR1 fragments, which could stimulate IL-8 production in the bronchial epithelial cells through Toll-like receptor 2.
The scientists inhibited the proteases in the airways in vivo by inhalation of alpha1-antitrypsin. This treatment restored CXCR1 expression and enhanced the bactericidal function in individuals suffering from cystic fibrosis.
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20.02.2008 | Anna Lena Marwedel 
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