Actin polymerization contributes to neutrophil chemotactic dysfunction following thermal injury

Abstract: The agent(s) and mechanism(s) responsible for suppression of neutrophil chemotaxis in association with major thermal injury have not been identified. We have proposed that the reduced random motility charac-terizing patients ’ cells may contribute to their generalized chemotactic dysfunction. Here we report that actin poly-merization may be responsible for the loss of neutrophil motility associated with major thermal injury. Using a fluorescent ligand specific for polymerized or filamentous actin (NBD-phallacidin) in conjunction with flow cytom-etry, we have discovered that peripheral blood and exu-date neutrophils from patients with major thermal injury contain increased levels of actin in a stably polymerized form. Because cyclic polymerization and depolymeriza-tion of actin is essential to cell motility, we suggest that actin polymerization may contribute in a major way to the attenuation of neutrophil random and chemotactic functions induced by major thermal injury. J. Leukoc