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LPS-induced neutrophilic inflammation and Bcl-2 expression in metaplastic mucous cells

¹Lovelace Respiratory Research Institute; ²University of New Mexico School of Medicine, and Veterans Administration Medical Center, Albuquerque, New Mexico 87108; ³Medical College of Georgia, Augusta, Georgia 30912; and Nicolaus Copernicus University, 87-100 Torun, Poland

Submitted 26 September 2002 ; accepted in final form 7 April 2003

Our previous studies show that Bcl-2, a regulator of apoptosis, may be involved in the reduction of mucous cell metaplasia (MCM) during recovery from inflammatory responses. The present study was to determine whether neutrophilic inflammation mediates Bcl-2 expression in mucous cells. Rats were intratracheally instilled with 50–1,000 µg of LPS. The number of neutrophils recovered by bronchoalveolar lavage (BAL) increased with the dose of LPS, and the percentage of Bcl-2-expressing cells increased with the numbers of neutrophils in the BAL. Depletion of neutrophils did not reduce MCM, but the percentage of Bcl-2-positive cells increased 1.8-fold in neutrophil-depleted compared with controls. Injection of rats with bezafibrate, an inducer of cytochrome P-450, doubled the number of neutrophils in the BAL, decreased MCM twofold compared with vehicle-injected controls, and reduced Bcl-2 expression. Bcl-2 mRNA levels decreased in a tracheal epithelial cell line treated with bezafibrate. These data demonstrate that Bcl-2 expression is independent of the number of neutrophils in the BAL and that bezafibrate may directly reduce Bcl-2 expression in epithelial cells.

airway epithelium; bezafibrate; apoptosis; lavaged cells; cytokines

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