Abstract
MO synthesize and secrete small amounts of C3. Studies were designed to determine if C3 production could be stimulated by LPS, a product present at sites of inflammation. Monocytes separated from normal human peripheral blood were cultured for 7 days in 5% human serum to promote maturation into MO35C3 production was assessed by hemolytic assay and incorporation of S-methionine into C3 protein. MO cultured in LPS (E.coli 0111: B4-Westphal extraction), 500 ng/ml, produced more C3 than controls: in 6 experiments increases were 15.1-fold for intracellular pro-C3 protein (range 5.4-32.6), 11.4-fold for extracellular native C3 protein (10.5-13.1), and 10.4-fold for extracellular C3 hemolytic activity (5.1-31.8). In contrast, LPS did not increase production of C2, lysozyme, lactate dehydrogenase, or total protein. Stimulation of C3 production was maximal after 24 hrs exposure to LPS. C3 production was increased by a polysaccharide-free mutant of LPS, but not by alkali-treated LPS, indicating that lipid A was responsible for stimulation. C3 production in human breast milk and bronchoalveolar MO was stimulated by LPS, but production in freshly adherent blood monocytes was not affected. The LPS-stimulated increase in C3 production was cycloheximide inhibitable, suggesting LPS increased translation of C3 protein stimulation. There was no alteration in post-translational processing. This potential for increased C3 synthesis in localized sites of inflammation may be important in resolution of the inflammation process.
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Strunk, R., Kunke, K. & Cole, F. LIPOPOLYSACCHARIDE (LPS) STIMULATES HUMAN AMOUNTS MACROPHAGES OF (MO) TO PRODUCE INCREASED AMOUNT OF THE THIRD COMPONENT OF COMPLEMENT (C3). Pediatr Res 18 (Suppl 4), 266 (1984). https://doi.org/10.1203/00006450-198404001-01037
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DOI: https://doi.org/10.1203/00006450-198404001-01037