Surfactant protein-a protects growing cells and reduces tumor
necrosis factor-[alpha] activity from lipopolysaccharide-stimulated
macrophages.
McIntosh, J. Clarke, Sabrena Mervin-Blake, Edward Conner, Jo Rae
Wright.
Departments of Pediatrics, Cell Biology, and Internal Medicine,
Duke University Medical Center
APStracts 3:0073L, 1996.
In addition to its effect on surfactant lipids, Surfactant Protein
(SP)-A promotes host defense. To define further the role of SP-A in
regulating immune cell function, we evaluated the effect of SP-A on
lipopolysaccharide (LPS)-activated alveolar macrophages in two
settings. First, co-cultured LPS-activated macrophages significantly
inhibited lung fibroblast growth, but SP-A (added daily) attenuated
this effect. Both LPS and SP-A acted via macrophages rather than
directly upon the fibroblasts, at least partially by affecting tumor
necrosis factor (TNF)-[alpha] activity. TNF-[alpha] reproduced the
growth suppression, anti-TNF-[alpha] antibodies attenuated the effect
of LPS-activated macrophages, and SP-A reduced TNF-[alpha] activity
in conditioned medium. Second, SP-A reduced TNF-[alpha] activity in
medium from isolated LPS-stimulated macrophages. SP-A's effects were
noted with or without serum, were dose-dependent and reversible, and
were seen with two different serotypes of smooth LPS. Equimolar
concentrations of IgG and C1q had no effect. Thus, SP-A both enhances
host defense and modulates immune functions of alveolar macrophages.
Received 3 October 1995; accepted in final form 29 April 1996.
APS Manuscript Number L293-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96