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pubmed:abstractText |
Complement activation with pneumococcal antigens was studied both in vitro and after injection of the antigens into rats. Whole pneumococci of various serotypes activated C3-C9 in rat serum treated with ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid, although serotypes differed greatly in the extent of activation. Some purified pneumococcal capsular polysaccharides also activated C3-C9 in rat serum, but only when the antigens were present in concentrations of 500 to 1,000 mug/ml. Much of the activation with capsular polysaccharides was eliminated by the use of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Activation of C3-C9 by capsular polysaccharides did not correlate with the level of reactivity observed with whole organisms of the same serotypes. After injection of 5 x 10(9) pneumococci (type 3 or type 4) intravenously into rats, there was a transient decline in serum C3-C9 activity, but there was no decline in C3-C9 levels after intravenous injection of 1,000 mug of type 3 or type 4 capsular polysaccharides. As determined by immunofluorescence, circulating capsular polysaccharide was deposited in several tissues, including the vascular endothelium and glomerular mesangium of the kidney. C3 was not detectable in these deposits, and there was no histological evidence of an inflammatory response. Capsular polysaccharides appear to be only weak activators of complement. Other pneumococcal antigens may be more important in the pathogenesis of hypocomplementemia in pneumococcal infection.
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