Abstract
Murine resident alveolar macrophages have very low numbers of complement receptors detectable by rosetting with erythrocyte complexes. These macrophages are relatively inactive in tests of complement- or antibody-mediated bacterial phagocytosis in vitro. It is not known whether these characteristics are intrinsic or are environmentally modulated. We found previously that rat bronchoalveolar lavage fluid or isolated rat surfactant lipid causes a unique and marked reduction in the ability of peritoneal macrophages to form rosettes with immunoglobulin G or complement containing erythrocyte complexes in vitro. In this study the antirosetting activity of rat surfactant was found to be due to its neutral lipid component and, specifically, to the free fatty acid (FFA) fraction of the neutral lipids. Rat surfactant contained a higher level of FFA than has been reported for canine, guinea pig, or human surfactant. Studies with pure FFA showed that activity in blocking macrophage Fc and complement receptors correlated with increasing unsaturation and chain length. A mixture of eight commercially available FFAs, representing the most abundant FFA in rat surfactant and consisting mostly of saturated FFA, had much less effect on rat macrophage receptors than the naturally occurring FFA mixture. These findings suggest that long-chain-unsaturated FFAs in rat surfactant are the most important for the antireceptor activity. The antireceptor activity of rat surfactant or FFA on peritoneal macrophage receptors in vitro and known intrinsic properties of murine alveolar macrophages could not be precisely correlated, suggesting that impaired binding of immune complexes by murine alveolar macrophages and a high level of FFAs in rat surfactant may be independent rather than causally related phenomena.
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