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Cleavage of CXCR1 on neutrophils disables bacterial killing in cystic fibrosis lung disease

() activates neutrophils via the chemokine receptors and . According to a recent study by Dominik Hartl from the Ludwig-Maximilian University in Munich, enhances the killing of bacteria by through , but not .

Cystic fibrosis leads frequently to colonisation of the airway by bacterial pathogens, although great numbers of and are present. Proteolytic activity in the airways of such individuals remained high, on 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 fragments, which could stimulate production in the bronchial epithelial cells through .
The scientists inhibited the proteases in the airways in vivo by inhalation of alpha1-antitrypsin. This treatment restored expression and enhanced the bactericidal function in individuals suffering from cystic fibrosis.

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