Activation of complement by opportunist pathogens and chemotypes of Salmonella minnesota.
Washed cells of Staphylococcus aureus, Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, and Salmonella minnesota chemotypes (S, Rb, and Re) were tested for their ability to activate the alternative complement pathway (ACP). Parameters of ACP activation were (i) conversion of C3 in 10 mM ethyleneglycol-bis-(beta-aminoethyl ether)-N,N1-tetraacetic acid-treated human serum supplemented with 2.5 mM MgCl2, (ii) lysis of glutathione-treated human erythrocytes in the presence of human serum, and (iii) C3 to C9 consumption in C4-deficient guinea pig serum. With the exception of S. minnesota Re and S. aureus, all of the strains were highly active in the test systems when compared with inulin. S. minnesota Re and S. aureus initiated C3 conversion in untreated human serum, suggesting that these microorganisms were capable of activating complement by a mechanism other than the ACP. These results provide direct evidence for ACP activation by opportunist gram-negative bacilli and refute the hypothesis that the lipid A moiety of the lipopolysaccharide cell wall is responsible for ACP activation.
D000328:Adult; D000818:Animals; D003181:Complement C4 / Q000172:deficiency; D003165:Complement System Proteins; D004533:Egtazic Acid / Q000494:pharmacology; D004912:Erythrocytes / Q000276:immunology; D004926:Escherichia coli / Q000276:immunology*; D006168:Guinea Pigs / Q000276:immunology; D006461:Hemolysis; D006801:Humans; D007106:Immune Sera; D007444:Inulin / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D011513:Proteus mirabilis / Q000276:immunology*; D011550:Pseudomonas aeruginosa / Q000276:immunology*; D012475:Salmonella / Q000276:immunology*; D013045:Species Specificity; D013211:Staphylococcus aureus / Q000276:immunology*
D003181:Complement C4; D007106:Immune Sera; D004533:Egtazic Acid; D007444:Inulin; D003165:Complement System Proteins; D008274:Magnesium