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Pulmonary surfactant lipids inhibit prostanoid production of guinea pig alveolar macrophages
Author(s) -
FöldesFilep éva,
Sirois Pierre,
Filep János G.
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.4.475
Subject(s) - biology , guinea pig , pulmonary surfactant , prostanoid , lung , pulmonary alveolus , immunology , microbiology and biotechnology , biochemistry , macrophage , medicine , endocrinology , in vitro , receptor
Changes in the amount and composition of pulmonary surfactant are important features of the adult respiratory distress syndrome. The goal of the present study was to investigate the effects of natural surfactant material and several of its lipid components on prostanoid production and superoxide generation by guinea pig alveolar macrophages. Natural surfactant (10–500 μ g/ml) inhibited (up to 65%) prostaglandin E 2 (PGE 2 ) and thromboxane B 2 (TxB 2 ) production elicited by platelet‐activating factor (PAF, 10 ‐6 M) and arachidonic acid (5 10 ‐6 M) but not fMet‐Leu‐Phe (10 ‐7 M). Dioleyl‐phosphatidylglycerol (diOPG, 1–100 μ g/ml) and dioleyl‐phosphatidylcholine (diOPC, 1–100 μ g/ml) prevented fMet‐Leu‐Phe‐ and PAF‐stimulated prostanoid release in a concentration‐dependent fashion with a maximal inhibition of 94%. DiOPC (100 μ g/ml) also inhibited arachidonic acid induced PGE 2 production by 67%. Phosphatidylcholine (100 μ g/ml) and sphingomyelin (10–100 μ g/ml) significantly attenuated TxB 2 production elicited by arachidonic acid. Neither PAF‐ nor fMet‐Leu‐Phe‐stimulated superoxide production was affected significantly by natural surfactant and its lipid components with the exception of phosphatidylcholine. At a concentration of 100 μ g/ml, phosphatidylcholine decreased superoxide production by about 57% in response to PAF. These results show that diOPC and diOPG are capable of inhibiting prostanoid production of guinea pig alveolar macrophages in response to inflammatory stimuli and suggest that a decrease in the diOPG and diOPC content of surfactant would lead to enhanced intrapulmonary formation of prostanoids and consequently to the deterioration of pulmonary function in the adult respiratory distress syndrome. J. Leukoc. Biol. 56: 475–480; 1994.