Toxicological Sciences 60, 152-164 (2001)
Copyright © 2001 by the Society of Toxicology
RESPIRATORY TOXICOLOGY |
Prior Exposure to Aged and Diluted Sidestream Cigarette Smoke Impairs Bronchiolar Injury and Repair
* Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine; University of California-Davis, Davis, California 95616-8732 and
Division of Statistics, University of California-Davis, Davis, California 95616-8732
The bronchiolar injury/repair response to naphthalene (NA) in mice includes acute distal airway epithelial injury that is followed by epithelial proliferation and redifferentiation, which result in repair of the epithelium within 14 days. To test whether prior exposure to aged and diluted sidestream cigarette smoke (TS) would alter the injury/repair response of the airway epithelium, adult mice were exposed to either filtered air (FA) or smoke for 5 days before injection with either corn oil carrier (CO) or naphthalene. Mice were killed 1 and 14 days after naphthalene injury. Lung and lobar bronchus were examined and measured using high-resolution epoxyresin sections. The control group (FACOFA) that was exposed to filtered air/corn oil/filtered air contained airway epithelium similar to untreated controls at all airway levels. The group exposed to tobacco smoke/corn oil/filtered air (TSCOFA) contained some rounded cells in the small airways and some expansion of the lateral intercellular space in the larger airways. Necrotic or vacuolated cells were not observed. As expected, the epithelium in the group exposed to filtered air/naphthalene/filtered air (FANAFA) contained many light-staining vacuolated Clara cells and squamated ciliated cells within distal bronchioles during the acute injury phase. Repair (including redifferentiation of epithelial cells and restoration of epithelial thickness) was nearly complete 14 days after injury. The extent of Clara cell injury, as assessed in lobar bronchi, was not different between the four groups. Although the FANAFA group contained greater initial injury in the distal airways at 1 day, the group exposed to tobacco smoke/naphthalene/filtered air (TSNAFA) had the least amount of epithelial repair at 14 days after naphthalene treatment; many terminal bronchioles contained abundant squamated undifferentiated epithelium. We conclude that tobacco smoke exposure prior to injury (1) does not change the target site or target cell type of naphthalene injury, since Clara cells in terminal bronchioles are still selectively injured; (2) results in slightly diminished acute injury from naphthalene in distal bronchioles; and (3) delays bronchiolar epithelial repair.
Key Words: cigarette smoking; tobacco smoke; bronchiolar injury and repair; epithelium; Clara cells; mice.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  G. L. Baker, M. A. Shultz, M. V. Fanucchi, D. M. Morin, A. R. Buckpitt, and C. G. Plopper Assessing Gene Expression in Lung Subcompartments Utilizing In Situ RNA Preservation Toxicol. Sci., January 1, 2004; 77(1): 135 - 141. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. P. M. Reddy and B. T. Mossman Role and regulation of activator protein-1 in toxicant-induced responses of the lung Am J Physiol Lung Cell Mol Physiol, December 1, 2002; 283(6): L1161 - L1178. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Fehrenbach, A. Fehrenbach, T. Pan, M. Kasper, and R.J. Mason Keratinocyte growth factor-induced proliferation of rat airway epithelium is restricted to Clara cells in vivo Eur. Respir. J., November 1, 2002; 20(5): 1185 - 1197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. N. Lango, K. F. Dyer, V. W. Y. Lui, W. E. Gooding, C. Gubish, J. M. Siegfried, and J. R. Grandis Gastrin-Releasing Peptide Receptor-Mediated Autocrine Growth in Squamous Cell Carcinoma of the Head and Neck J Natl Cancer Inst, March 6, 2002; 94(5): 375 - 383. [Abstract] [Full Text] [PDF]
|
|