Cefodizime (HR 221) potentiation of human neutrophil oxygen-independent bactericidal activity.
The enhanced bactericidal activity of human neutrophils induced by cefotaxime and cefodizime, two methoxy-imino-amino- 2-thiazolyl cephalosporins, is linked to the cell stimulation of oxygen-dependent and oxygen-independent killing systems, respectively. Cefotaxime enhances both the killing and the oxidative response of neutrophils to opsonized particulate stimuli (bacteria for both activities and opsonized zymosan for the oxidative burst). These effects were not observed with non-opsonized particles (bacteria or zymosan) or soluble stimuli. On the contrary, cefodizime enhances killing of opsonized and non-opsonized bacteria by neutrophils regardless of treatment with phenylbutazone which blocks neutrophil oxidative metabolism. Cefodizime does not universally alter the oxidative burst induced by various stimuli, but has been shown to enhance the bactericidal activity of crude extracts of neutrophil granules. The data suggest that cefodizime and non O2-dependent killing systems of neutrophils cooperate in killing bacteria.
D002439:Cefotaxime / Q000031:analogs & derivatives* / Q000494:pharmacology*; D006801:Humans; D007711:Klebsiella pneumoniae / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D009895:Opsonin Proteins; D010101:Oxygen Consumption; D010587:Phagocytosis / Q000187:drug effects*; D010653:Phenylbutazone / Q000494:pharmacology; D013211:Staphylococcus aureus / Q000187:drug effects; D013481:Superoxides / Q000378:metabolism
D009895:Opsonin Proteins; D013481:Superoxides; D010653:Phenylbutazone; D002439:Cefotaxime; C033356:cefodizime