Stimulation of complement component C3 synthesis in macrophagelike cell lines by group B streptococci.
Complement levels and complement activation are key determinants in streptococcus-induced inflammatory responses. Activation of macrophage functions, such as complement synthesis, by group B streptococci (GBS) was examined as a possible component of GBS-induced chronic inflammation. Using an enzyme-linked immunosorbent assay, secreted C3 from mouse macrophagelike cell lines (PU5-1.8 and J774A.1) was monitored after cultivation with GBS. Whole, heat-killed GBS (1 to 10 CFU per macrophage) of both type Ia and III strains induced 25 to 300% increases in secreted C3 in both cell lines after a 24-h cultivation. GBS-treated cell lines exhibited increases in secreted lysozyme (10%) and in cellular protein (25 to 50%). Inhibition of macrophage phagocytosis by cytochalasin B inhibited GBS stimulation of C3. Purified cell walls of GBS type III strain 603-79 (1 to 10 micrograms/ml) also enhanced C3 synthesis. Local enhancement of macrophage C3 production by ingested streptococci or by persistent cell wall antigens may serve to promote chronic inflammatory responses.
D000818:Animals; D002460:Cell Line; D002473:Cell Wall / Q000276:immunology; D003176:Complement C3 / Q000096:biosynthesis*; D003571:Cytochalasin B / Q000494:pharmacology; D007249:Inflammation / Q000276:immunology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D014176:Protein Biosynthesis; D013290:Streptococcal Infections / Q000276:immunology; D013292:Streptococcus agalactiae / Q000276:immunology*
D003176:Complement C3; D003571:Cytochalasin B