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 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.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Hasslen SR,Ahrenholz DH,Solem LD,Nelson RDdoi
10.1002/jlb.52.5.495subject
Has Abstractpub_date
1992-11-01 00:00:00pages
495-500issue
5eissn
0741-5400issn
1938-3673journal_volume
52pub_type
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