title: Antibody-independent classical pathway-mediated opsonophagocytosis of type Ia, group B streptococcus.
abstract: The opsonophagocytic requirements of human sera containing endogenous complement for a variety of type Ia, and group B streptococcal strains were defined. Significant reduction (>==90%) in colony-forming units was noted after a 40-min incubation for the highly encapsulated, mouse-passed prototype strain 090 by sera containing moderate to high concentrations of antibody to type Ia polysaccharide (mean, 16.5 mug/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 mug/ml). This absolute requirement for a critical amount of specific antibody in promoting opsonophagocytic killing of strain 090 was not found when 18 fresh clinical type Ia isolates were tested. In antibody-deficient and agammaglobulinemic sera, respectively, mean reductions in colony-forming units of 94 and 95% were seen for fresh clinical isolates, whereas strain 090 was not killed by polymorphonuclear leukocytes in the presence of these sera. All strains required a considerable amount of specific antibody for alternative pathway-mediated opsonophagocytosis. That opsonophagocytic killing of clinical type Ia isolates was mediated by the classical pathway in a nonantibody-dependent fashion was shown when MgEGTA chelation of agammaglobulinemic serum or use of serum deficient in C2 resulted in bacterial growth. The addition of C2 to C2-deficient serum restored bactericidal activity of this serum. These experiments indicate that substances other than the exposed surface of the type Ia capsular polysaccharide initiate classical pathway-mediated opsonophagocytosis of clinical isolates of type Ia, group B streptococci by human sera in the absence of immunoglobulin. Perhaps, a deficiency in classical complement pathway function is critical to the susceptibility of neonates to type Ia, group B streptococcal disease.
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology / Q000502:physiology*; D000918:Antibody Specificity; D003167:Complement Activation; D003175:Complement C2 / Q000172:deficiency; D003171:Complement Pathway, Classical; D006168:Guinea Pigs; D006801:Humans; D051379:Mice; D008815:Mice, Inbred Strains; D009895:Opsonin Proteins / Q000276:immunology / Q000502:physiology*; D010587:Phagocytosis; D011135:Polysaccharides, Bacterial / Q000276:immunology / Q000502:physiology; D011817:Rabbits; D013290:Streptococcal Infections / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D013292:Streptococcus agalactiae / Q000276:immunology / Q000472:pathogenicity; D014774:Virulence
chemical_list: D000907:Antibodies, Bacterial; D003175:Complement C2; D009895:Opsonin Proteins; D011135:Polysaccharides, Bacterial