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Am J Physiol Lung Cell Mol Physiol 283: L612-L618, 2002. First published April 12, 2002; doi:10.1152/ajplung.00483.2001
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Vol. 283, Issue 3, L612-L618, September 2002

Bradykinin increases IL-8 generation in airway epithelial cells via COX-2-derived prostanoids

Helen C. Rodgers, Linhua Pang, Elaine Holland, Lisa Corbett, Simon Range, and Alan J. Knox

Division of Respiratory Medicine, City Hospital, Nottingham NG5 1PB, United Kingdom

Interleukin (IL)-8, the C-X-C chemokine, is a potent neutrophil chemoattractant that 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 a non-cystic fibrosis (A549) and cystic fibrosis epithelial cell line (CFTE29<UP><SUB>o</SUB><SUP>−</SUP></UP>) that was inhibited by the nonselective cyclooxygenase (COX) inhibitor indomethacin and the COX-2 selective inhibitor NS-398. COX-2 was the only isoform of COX expressed in both cell lines. Furthermore, the COX substrate arachidonic acid and exogenous prostaglandin E2 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 airway diseases characterized by neutrophilic inflammation such as cystic fibrosis or chronic obstructive pulmonary disease.

interleukin-8; lung; chemokines; inflammation; cystic fibrosis; cyclooxygenase-2


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