Actin polymerization contributes to neutrophil chemotactic dysfunction following thermal injury.
Actin polymerization contributes to neutrophil chemotactic dysfunction following thermal injury.
复制标题
肌动蛋白聚合导致热损伤后中性粒细胞趋化功能障碍。
DOI：
10.1002/jlb.52.5.495
复制
发表时间：
1992
影响因子：
5.5
通讯作者：
Nelson,RD
中科院分区：
文献类型：
--
作者：
Hasslen,SR;Ahrenholz,DH;Solem,LD;Nelson,RD
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 characterizing patients' cells may contribute to their generalized chemotactic dysfunction. Here we report that actin polymerization 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 cytometry, we have discovered that peripheral blood and exudate neutrophils from patients with major thermal injury contain increased levels of actin in a stably polymerized form. Because cyclic polymerization and depolymerization 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.
