Complement and Antibody in Neutrophil-Mediated Killing of Type V Group B Streptococcus

Serious infections caused by type V group B streptococci (GBS) are increasing. The requirements for antibody, complement, and neutrophil receptors in the killing of 12 clinical type V GBS isolates were investigated. When tested at concentrations of 33%, 5% and 1%, a human serum pool promoted neutrop...

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Bibliographic Details
Published in:The Journal of infectious diseases 1994-07, Vol.170 (1), p.88-93
Main Authors: Hall, Mary A., Hickman, Melissa E., Baker, Carol J., Edwards, Morven S.
Format: Article
Language:English
Subjects:
Animals
Antibodies
Antibodies, Bacterial - immunology
Bacterial diseases
Biological and medical sciences
Blood
Cells, Cultured
Complement System Proteins - immunology
Fc receptors
Human bacterial diseases
Humans
Infants
Infections
Infectious diseases
Major Articles
Medical sciences
Mice
Monoclonal antibodies
Neutrophils
Neutrophils - cytology
Neutrophils - immunology
Receptors
Staphylococcal infections, streptococcal infections, pneumococcal infections
Streptococcus agalactiae
Streptococcus agalactiae - immunology
T tests
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Summary:Serious infections caused by type V group B streptococci (GBS) are increasing. The requirements for antibody, complement, and neutrophil receptors in the killing of 12 clinical type V GBS isolates were investigated. When tested at concentrations of 33%, 5% and 1%, a human serum pool promoted neutrophil-mediated killing of the 12 isolates at a mean of 83% ± 9%, 77% ± 17%, and 14% ± 28%, respectively. Addition of heated immune rabbit serum to the 5% or 1% pool increased killing significantly (97% ± 2% or 80% ± 15%, respectively, P < .01). With hypogammaglobulinemic serum, complement-mediated killing ranged from 74% ± 2% for a strain designated resistant to 98% ± 1% for a strain designated sensitive. Neutrophil-mediated killing was not altered by use of human sera deficient in C4 or C7 but was reduced significantly with C3-deficient serum (P < .05). Maximal inhibition of neutrophil-mediated killing was observed by monoclonal antibody blockade of complement receptor (CR) 3 alone or in combination with CRI or Fe receptor III. Thus, C3 is required and specific antibody promotes neutrophil-mediated killing of type V GBS. Neutrophil CR3 and either CRI or Fe receptor III optimize phagocytosis. A number of host responses function in concert to effect optimal neutrophil-mediated killing of clinical isolates of type V GBS.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/170.1.88