Group A streptococcal peptidoglycan-polysaccharide inhibits phagocytic activity of human polymorphonuclear leukocytes.
Injection of sterile aqueous preparations of the peptidoglycan-polysaccharide of group A streptococci (PG-APS) produces chronic inflammation in several animal models. Chronic bacterial infection may be involved in some aspects of the pathogenesis of inflammation associated with the accumulation of PG-APS. Accordingly, the effect of PG-APS on human neutrophil (polymorphonuclear leukocyte [PMN]) bactericidal activity was studied with the supposition that this interaction may contribute to the inflammation observed. Concentrations of PG-APS greater than 10 micrograms/ml inhibited the ability of PMNs to kill Staphylococcus aureus. This inhibition was not due to a cytotoxic effect of PG-APS on PMNs, nor did PG-APS inhibit PMN metabolism required for the formation of microbicidal oxygen reduction products. PG-APS concentrations of 10 micrograms/ml or greater in the presence of 10% normal serum inhibited the attachment of bacteria to PMNs by 49% as compared with control cell populations. The concentrations of PG-APS required to inhibit uptake of Staphylococcus aureus were identical to those required for inhibition of PMN bactericidal activity. This inhibition did not occur in the presence of serum-free medium or medium with sera that had been heated to inactivate complement. These results show that PG-APS interacts with serum to inhibit PMN-mediated killing of S. aureus, most probably by interfering with bacterial uptake.
D003773:Dental Plaque / Q000276:immunology / Q000382:microbiology; D006801:Humans; D009504:Neutrophils / Q000276:immunology*; D010101:Oxygen Consumption; D010457:Peptidoglycan / Q000276:immunology*; D010587:Phagocytosis; D013211:Staphylococcus aureus / Q000276:immunology; D013297:Streptococcus pyogenes / Q000276:immunology*; D013298:Streptococcus sanguis / Q000276:immunology*
D010457:Peptidoglycan