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1 Department of Pathophysiology, Lovelace Respiratory Research Institute, Albuquerque, NM, USA
2 Department of Medicine, University of New Mexico School of Medicine and Veteran's Administration Medical Center, Albuquerque, NM, USA
3 Department of Physiology, Medical College of Georgia, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: ytesfaig{at}lrri.org.
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 to 1000 µg 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 to controls. Injection of rats with bezafibrate, an inducer of cytochrome P-450, doubled the number of neutrophils in the BAL, decreased MCM 2-fold compared to 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 bezafibrate may directly reduce Bcl-2 expression in epithelial cells.
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