Effect of surfactant on basal and silica-induced eicosanoid
production by the alveolar macrophage.
Kuhn, Douglas C., and Laurence M. Demers.
Department of Pathology, The Pennsylvania State University College
of Medicine, The M.S. Hershey Medical Center, Hershey, PA 17033
APStracts 2:0055L, 1995.
Inflammation and fibrosis subsequent to the inhalation of certain
mineral dust particles has been suggested to result from the
activation of eicosanoid synthesis by the alveolar macrophage (AM).
In order to determine if surfactant modifies dust-induced generation
of eicosanoids by the AM, we evaluated the effect of the surfactant
lipid dipalmitoyl lecithin (DPL) on the production of eicosanoids by
rat AM exposed to respirable silica dust in vitro. During the first
24-hr exposure period, DPL alone significantly increased basal
production of eicosanoids but completely inhibited silica-induced
thromboxane A2 synthesis. In contrast, leukotriene B4 (LTB4)
production was only partially reduced by DPL. During a second 24-hr
exposure period, LTB4 production in response to the highest dose of
silica remained significantly elevated in the presence of DPL.
Similar results were obtained when the surfactant preparation
Survanta was evaluated. These results suggest that 1) DPL and
Survanta independently activate AM eicosanoid production, 2) DPL and
Survanta modulate the response of the AM to silica dust and 3) LTB4
may be the most important eicosanoid mediator of the long-term
effects of silica dust exposure on lung pathophysiology.
Received 20 June 1994; accepted in final form 28 March 1995.
APS Manuscript Number L180-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.