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Research Article Free access | 10.1172/JCI110463
Department of Pediatrics, Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030
Channing Laboratory and Departments of Medicine, Peter Bent Brigham, Division of Affiliated Hospital Center Inc., Beth Israel Hospital, Boston, Massachusetts 02115
Harvard Medical School, Boston, Massachusetts 02115
Find articles by Baker, C. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030
Channing Laboratory and Departments of Medicine, Peter Bent Brigham, Division of Affiliated Hospital Center Inc., Beth Israel Hospital, Boston, Massachusetts 02115
Harvard Medical School, Boston, Massachusetts 02115
Find articles by Edwards, M. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030
Channing Laboratory and Departments of Medicine, Peter Bent Brigham, Division of Affiliated Hospital Center Inc., Beth Israel Hospital, Boston, Massachusetts 02115
Harvard Medical School, Boston, Massachusetts 02115
Find articles by Webb, B. in: JCI | PubMed | Google Scholar
Department of Pediatrics, Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77030
Channing Laboratory and Departments of Medicine, Peter Bent Brigham, Division of Affiliated Hospital Center Inc., Beth Israel Hospital, Boston, Massachusetts 02115
Harvard Medical School, Boston, Massachusetts 02115
Find articles by Kasper, D. in: JCI | PubMed | Google Scholar
Published February 1, 1982 - More info
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 μg/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 μg/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.
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