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 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 Biol

authors

Hasslen SR,Ahrenholz DH,Solem LD,Nelson RD

doi

10.1002/jlb.52.5.495

subject

Has Abstract

pub_date

1992-11-01 00:00:00

pages

495-500

issue

5

eissn

0741-5400

issn

1938-3673

journal_volume

52

pub_type

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