Neutrophils enhance removal of ozone-injured alveolar epithelial
cells in vitro.
Cheek, Jeffrey M., Ruth J. McDonald, Lisa Rapalyea, Brian K.
Tarkington, and Dallas Hyde.
Department of Veterinary Anatomy, Physiology and Cell Biology and
Department of Pediatrics and California Regional Primate Research
Center, University of California, Davis, CA 95616
APStracts 2:0100L, 1995.
Following acute exposure to oxidant gases in vivo, migration and
accumulation of inflammatory cells in pulmonary epithelium coincides
with epithelial cell necrosis. The present study was designed to
quantitatively test the hypothesis that quiescent neutrophils enhance
the removal of oxidant-injured pulmonary epithelial cells following
exposure to ozone in vitro. Primary isolated rat alveolar type II
cells were cultured as monolayers using serum-free medium. Following
exposure to 0.1-0.5 ppm ozone for 0.5 hr, apical sides of monolayers
were administered either fresh nutrient medium only or medium
containing quiescent human neutrophils. Monolayer bioelectric
properties and cellular uptake of vital dye were recorded from 5-48
hr following ozone exposure. Ozone dose-dependent increases in
monolayer permeability were associated with proportionally higher
numbers of injured epithelial cells. However, the direction and
magnitude of neutrophil effects on monolayer permeability following
ozone exposure were dependent on ozone concentration. Furthermore,
neutrophil-treated monolayers exposed to 0.1 ppm ozone had
significantly fewer attached cells positive for uptake of vital dye
relative to monolayers exposed to the low level of ozone only; this
effect was ablated with increasing ozone concentration. These data
suggest that at high levels of ozone neutrophils may exacerbate
injury to oxidant-impaired epithelial cells, while the presence of
neutrophils following exposure to ambient concentrations of ozone may
expedite the restoration of epithelial barrier function. We conclude
that, by enhancing the removal of injured cells, neutrophils may
facilitate the repair of centriacinar epithelium after ozone exposure
in vivo.
Received 18 July 1994; accepted in final form 9 May 1995.
APS Manuscript Number L201-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.