Abstract
The chemotaxis of neutrophils is modulated by serum factors, tissue factors, bacterial products and other substances. In vivo, these factors may act in concert with each other to modify neutrophil movement. The effect of aggregated .gamma. globulin-activated serum (AS) [human], bacterial factors and endotoxin alone or in combination with each other, on human neutrophil chemotaxis was examined. Exposure of neutrophils to AS resulted in deactivation to AS but not to Escherichia coli or Staphylococcus epidermis culture filtrate [CF]. Exposure of neutrophils to S. epidermis or E. coli CF or E. coli endotoxin resulted in deactivation to AS or [complement component] C5a but not to E. coli or S. epidermis CF. Addition of endotoxin to AS or C5a resulted in inhibition of chemotaxis by untreated neutrophils toward this combination as compared with AS alone. Separate mechanisms may be involved when serum or bacterial chemotactic factors initiate human neutrophil chemotaxis. The potent but specific inhibitory effect of endotoxin on chemotaxis toward AS may be of clinical significance.