The role of complement in the localization of pneumococci in the splanchnic reticuloendothelial system during experimental bacteremia.

Published

Journal Article

Pneumococci activate the alternative complement (C) pathway in the absence of demonstrable antibody in normal guinea pig serum. They also activate the classical C pathway in the presence of type-specific antibody and perhaps through other mechanisms as well. A quantitative examination was undertaken of the roles of these 2 pathways of C activation in the splanchnic sequestration of 125I-labeled pneumococci, using a-guinea pig model of pneumococcal bacteremia. Normal unimmunized guinea pigs (NIH-GP) localized more than 3 times as many pneumococci to the liver as the spleen during a period when exponential bloodstream clearance was occurring. C4-deficient guinea pigs (C4D-GP) and cobra venom factor-treated guinea pigs (CVF-GP) showed progressively fewer pneumococci cleared by the liver with concomitant increases in the extent of splenic uptake, demonstrating the important role of C in the clearance of bacteria in the unimmunized animal. Immunization of guinea pigs brought about an increase in pneumococcal sequestration by the liver in NIH and C4D-GP but did not affect the localization pattern of CVF-GP. A comparison of reticuloendothelial system (RES) localization patterns with the rate of removal of bacteria from the bloodstream showed a highly significant correlation between increases in splenic sequestration and persistence of bacteremia. Thus, opsonization by C is an important determinant of the RES clearance of pneumococci. Unlike RBC clearance, where C plus IgM leads to hepatic localization, and C plus IgG tends to produce splenic localization, C in the presence or absence of type-specific antibody tends to cause hepatic localization of pneumococci. When C-mediated opsonic activity is less than optimal, the slower clearance of bacteremia that results is accompanied by an increased dependence on splenic sequestration of pneumococci.

Full Text

Cited Authors

  • Brown, EJ; Hosea, SW; Frank, MM

Published Date

  • June 1981

Published In

Volume / Issue

  • 126 / 6

Start / End Page

  • 2230 - 2235

PubMed ID

  • 7229372

Pubmed Central ID

  • 7229372

International Standard Serial Number (ISSN)

  • 0022-1767

Language

  • eng

Conference Location

  • United States