AJP - Lung Cellular and Molecular Physiology, Vol 269, Issue 2 165-L170, Copyright © 1995 by American Physiological Society
Effect of surfactant on basal and silica-induced eicosanoid production by the alveolar macrophage
D. C. Kuhn and L. M. Demers
Department of Pathology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey 17033, USA.
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). 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-h 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-h 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.
