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Articles in PresS, published online ahead of print April 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00483.2001
Submitted on December 17, 2001
Accepted on April 9, 2002
1 Respiratory Medicine, Nottingham University, Nottingham, Notts, United Kingdom
* To whom correspondence should be addressed. E-mail: alan.knox{at}nottingham.ac.uk.
IL-8, the CXC chemokine, is a potent neutrophil chemoattractant which has been implicated in a number of inflammatory airway diseases such as cystic fibrosis. Here we tested the hypothesis that bradykinin, an inflammatory mediator and chloride secretagogue, would increase IL-8 generation in airway epithelial cells through autocrine generation of endogenous prostanoids. Bradykinin increased IL-8 generation in both non-cystic fibrosis (A549) and cystic fibrosis (CFTE29o-) epithelial cell lines, which was inhibited by the non-selective COX inhibitor indomethacin and the COX-2 selective inhibitor NS-398. COX-2 was the only isoform of cyclo-oxygenase expressed in both cell lines. Furthermore, the COX substrate arachidonic acid and exogenous PGE2 both increased IL-8 release in A549 cells. These results suggest that bradykinin may contribute to neutrophilic inflammation in the airway by generation of IL-8 from airway epithelial cells. The dependence of this response on endogenous production of prostanoids by COX-2 suggests that selective COX-2 inhibitors may have a role in the treatment of airways diseases characterised by neutrophilic inflammation such as cystic fibrosis or chronic obstructive pulmonary disease.
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