Influence of serum-derived chemotactic factors and bacterial products on human neutrophil chemotaxis

Abstract

The chemotaxis of neutrophils has been shown to be modulated by serum factors, tissue factors, bacterial products, and a host of other substances. In vivo, these factors may act in concert with each other to modify neutrophil movement. We examined the effect of aggregated gamma globulin-activated serum (AS), bacterial factors, and endotoxin either alone or in combination with each other, on human neutrophil chemotaxis. Exposure of neutrophils to AS resulted in deactivation to AS but not to Escherichial coli or Staphylococcus epidermis culture filtrate. Exposure of neutrophils to S. epidermis or E. coli CF or E. coli endotoxin resulted in deactivation to AS or C5a but not to E. coli or S. epidermis culture filtrate. Addition of endotoxin to AS or C5a resulted in inhibition of chemotaxis by untreated neutrophils toward this combination as compared with AS alone. These results suggest that separate mechanisms may be involved when serum or bacterial chemotactic factors initiate human neutrophil chemotaxis. Furthermore, the potent but specific inhibitory effect of endotoxin on chemotaxis toward AS may be of clinical significance.