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1 Department of Chest Medicine, Taiepi Veterans General Hospital, Taipei, Taiwan, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan, Taiwan
2 Division of Chest Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan, Taiwan
3 Department of Chest Medicine, Taiepi Veterans General Hospital, Taipei, Taiwan, Taiwan
4 Division of Chest Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, Taiwan
* To whom correspondence should be addressed. E-mail: dwperng{at}vghtpe.gov.tw.
The responses of airway epithelium following exposure to neutrophil elastase were investigated. Human bronchial epithelial cells were explanted on insert surfaces of a modified air-liquid interface culture system to which NE was added to stimulate epithelial cells. PGE2 release significantly increased within ten minutes of incubation with NE and peaked three hours after NE (20 µg/ml) stimulation. This action required proteolytic activity as 
1-antitrypsin blocked NE-induced PGE2 release. The production of PGE2 was also inhibited by indomethacin, a selective COX-2 inhibitor, celecoxib, and dexamethasone. Moreover, the mRNA expression for COX-2 relative to that for a housekeeping gene was approximately eight-fold that of the unstimulated cells. Dexamethasone inhibited COX-2 gene transcription. We further observed that NE-induced PGE2 release involved activation of p44/42, but not p38, MAP kinases. Such p44/42 MAP kinases were rapidly phosphorylated, with the concentration of phosphorylated p44/42 MAP kinases peaking at ten minutes after stimulation and declining in culture at 90 minutes. The specific p44/42 MAP kinase inhibitor, UO126, completely blocked p44/42 phosphorylation and, subsequently, PGE2 production. The airway epithelium may play important bronchoprotective and immunomodulatory roles in chronic neutrophilic inflammation.
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