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 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 CR1 or Fc receptor III. Thus, C3 is required and specific antibody promotes neutrophil-mediated killing of type V GBS. Neutrophil CR3 and either CR1 or Fc 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.
Hall
M A
MA
Dept. of Pediatrics, Baylor College of Medicine, Houston, TX 77030.
Hickman
M E
ME
Baker
C J
CJ
Edwards
M S
MS
D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology*; D002478:Cells, Cultured; D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D051379:Mice; D009504:Neutrophils / Q000166:cytology / Q000276:immunology*; D013292:Streptococcus agalactiae / Q000276:immunology*
D000907:Antibodies, Bacterial; D003165:Complement System Proteins