Evidence for a reversible functional state of neutrophil chemotactic deactivation.
Neutrophils pretreated with a chemotactic factor become deactivated, that is, unresponsive to a subsequent chemotactic stimulus. A decay of surface esterase activity, an increased adhesiveness, an auto-oxidative damage of the cell structures and microtubule hyperpolymerization have been previously proposed as the cause of the chemotactic deactivation. To further understand the cellular mechanisms involved in this process, we have studied the locomotory behaviour of deactivated neutrophils in an experimental system allowing differentiation among the various types of migratory cellular response to chemotactic factors. Thus, we have found that deactivated neutrophils retain a normal capacity of random locomotion, but entirely lose their true chemotactic responsiveness. Diamide, which disrupts assembled microtubules in concanavalin A-treated cells, was able to completely restore the true chemotactic response of deactivated cells. These observations suggest that neutrophil deactivation is a reversible cellular event dependent on the functional state of the microtubular system.
D002465:Cell Movement / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D003958:Diamide / Q000494:pharmacology; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*
D003958:Diamide