Alterations in surfactant associated protein a (sp-a) after acute
exposure to ozone.
Su, Wei Yi, and Terry Gordon.
Department of Environmental Medicine, New York University Medical
Center, Long Meadow Road, Tuxedo, New York 10987
APStracts 3:0003A, 1996.
The surfactant layer covering the gas exchange region of the lung
serves as the initial site of interaction with inhaled oxidant gases.
Among the endogenous compounds potentially vulnerable to oxidative
injury are surfactant associated proteins. This study focused on the
effect of ozone on surfactant associated protein A (SP-A) function,
content, and gene expression. To determine the time course of
response to ozone, guinea pigs were exposed to 0.2 to 0.8 ppm ozone
for 6 hr and sacrificed up to 120 hr postexposure. To determine the
effect of repeated exposure, animals were exposed to 0.8 ppm ozone
for 6 hr/day and sacrificed on days 3 and 5. A significant increase
in surfactant's ability to modulate phorbol myristate acetate-induced
respiratory burst in naive macrophages was observed at 24 hr after a
single 0.8 ppm ozone exposure. Because neutralizing antibodies to SP
-A blunted this stimulatory effect, we hypothesized that ozone
enhanced SP-A's modulatory role in macrophage function. This
alteration in function was accompanied by an influx of inflammatory
cells and only marginal changes in SP-A levels as determined by
ELISA. No significant changes in steady state levels of SP-A mRNA
were observed after single or repeated exposure to ozone. Thus, the
inflammation that accompanies in vivo ozone exposure may result in a
change in the structure and thus functional role of SP-A in
modulating macrophage activity.
Received 1 May 1995; accepted in final form 3 November 1995.
APS Manuscript Number A466-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96