Hypersusceptibility of penicillin-treated group B streptococci to bactericidal activity of human polymorphonuclear leukocytes.
Pretreatment of serotype Ib group B streptococci with benzylpenicillin, other beta-lactam antibiotics, or vancomycin increased the susceptibility of these bacteria to the bactericidal activity of a mixture of human polymorphonuclear leukocytes and normal human serum. Increased susceptibility of the bacteria to killing by phagocytes was elicited even by exposure to subinhibitory levels of the beta-lactam antibiotics. Inhibitors of protein synthesis did not induce such susceptibility. We investigated the possible biochemical basis of penicillin-induced susceptibility to phagocytosis. Penicillin treatment induced the release of substantial quantities of group B streptococcal surface components into the growth medium (lipoteichoic acid, lipid, and capsular polysaccharide). Labeling of the live streptococci with 3H-labeled penicillin was used to evaluate the effect of exposure to subinhibitory concentrations of this antibiotic on the penicillin-binding proteins. Our results suggested that beta-lactam antibiotics and components of the immune system may act in concert to eliminate invading bacteria.
D000328:Adult; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins; D002352:Carrier Proteins / Q000378:metabolism; D002473:Cell Wall / Q000378:metabolism; D006602:Hexosyltransferases; D006801:Humans; D002267:Muramoylpentapeptide Carboxypeptidase; D009504:Neutrophils / Q000276:immunology*; D010400:Penicillin G / Q000494:pharmacology*; D046915:Penicillin-Binding Proteins; D010458:Peptidyl Transferases; D010587:Phagocytosis; D013292:Streptococcus agalactiae / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D002352:Carrier Proteins; D046915:Penicillin-Binding Proteins; D010458:Peptidyl Transferases; D006602:Hexosyltransferases; D002267:Muramoylpentapeptide Carboxypeptidase; D010400:Penicillin G