The critical role of complement in experimental pneumococcal sepsis.
Using a guinea pig model fo bacteremia due to Streptococcus pneumoniae serotype 7, opsonization by the classical and alternative pathways of complement activation was studied in immune and nonimmune animals. Depletion of the alternative complement pathway and complement components C3-C9 resulted in a significant, lethal defect of intravascular clearance in both normal and immune animals. Preopsonization corrected the initial clearance defect in complement-depleted animals. Maximal rates of clearance of bacteremia occurred in immune, normal animals, Immune, C4-deficient animals had clearance curves similar to normal, nonimmune animals. Thus, optimal clearance of pneumococcal bacteremia requires an  intact alternative an classical pathway of complement activation. In the nonimmune animal, the alternative pathway provides the primary host defense against infection, whereas after immunization, optimal clearance of bacteremia requires an intact classical pathway of complement activation. However, immunization does not alter the lethal clearance defect in complement-depleted animals.
D000818:Animals; D001770:Blood Bactericidal Activity; D003170:Complement Pathway, Alternative; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000276:immunology*; D006168:Guinea Pigs; D011008:Pneumococcal Infections / Q000276:immunology*; D018805:Sepsis / Q000276:immunology*; D013296:Streptococcus pneumoniae / Q000276:immunology; D014774:Virulence
D003165:Complement System Proteins