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The human monocyte-like cell line, U937, was utilized as a model system toassess the influence of lipopolysaccharides (LPS) from Escherichia coli and other immunomodulatoryagents on the biosynthesis of complement component C3 by monocytoid cells.The amount of C3 accumulated in the medium of cultured cells was measured by an enzymelinkedimmunoabsorbent assay (ELISA). In the presence of LPS (0.01 and 0.10 μg/ml) C3production by U937 cells was increased by 2- and 5-fold, respectively. C3 production was alsoincreased in the presence of lymphokine-containing supernatants obtained from humanperipheral blood mononuclear cells after their stimulation with concanavalin A-sepharose.Human γ-interferon (50-500 units/ml) stimulated C3 production by U937 cells. Stimulationof C3 production by LPS or mononuclear cell supernatants was blocked by cycloheximide.LPS (0.10 and 1.0 μg/ml) also stimulated PGE(2) production by U937 cells but failed toincrease PGE(2) at the lowest concentration (0.01 μg/ml) shown to increase C3 biosynthesis.Although exogenous PGE(1) (10^–7 and 10^–6 M) promoted a small increase in C3 production, theeffect of LPS was not decreased by a concentration of indomethacin (10^–6 M) that inhibitedbiosynthesis of PGE(2). Therefore, LPS-induced C3 synthesis is not mediated by an increase inPGE(2) in U937 cells. In summary, these observations suggest that C3 biosynthesis by monocytes/macrophages can be modulated by mediators of cellular immune responses found in themicroenvironment of a localized inflammatory reaction.
Complement – Karger
Published: Jan 1, 2017
Keywords: Monocyte; Macrophage; Complement (C3); LPS; PGE(2)
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