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Interleukin‐8 induces changes in human neutrophil actin conformation and distribution: relationship to inhibition of adhesion to cytokine‐activated endothelium
Author(s) -
Westlin William F.,
Kiely JeanneMarie,
Gimbrone Michael A.
Publication year - 1992
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.52.1.43
Subject(s) - cytochalasin d , cytochalasin b , cytochalasin , biology , microbiology and biotechnology , chemotaxis , platelet activating factor , actin , adhesion , microfilament , endothelium , cytoskeleton , biophysics , cytokine , n formylmethionine leucyl phenylalanine , immunology , biochemistry , chemistry , in vitro , cell , endocrinology , receptor , organic chemistry
Interleukin‐8 (IL‐8) induces diverse biological responses in neutrophils, including inhibition of adhesion to cytokine‐activated endothelium, which we have termed the leukocyte adhesion inhibition (LAI) effect. Pretreatment of neutrophils with cytochalasin B abolished the LAI effect of IL‐8, suggesting a microfilament‐dependent mechanism. Interleukin‐8 induced a rapid increase (≤ 15 s) in the polymerization of actin filaments in human neutrophils that was blocked by pretreatment with cytochalasin B. F‐actin depolymerization occurred gradually at a rate inversely proportional to IL‐8 concentration. This temporal pattern of actin polymerization‐depolymerization was similar to that induced by other chemotactic factors such as C5a and N ‐formylmethionyl‐leucyl‐phenylalanine, which also exhibit a marked LAI effect, but the lipid mediators, leu‐kotriene B 4 and platelet‐activating factor, lack any significant LAI effect. Scanning confocal microscopy demonstrated that neutrophil actin microfilaments undergo a dramatic rearrangement prior to detachment of the neutrophil from a surface. We suggest that the ability of IL‐8 and certain other leukocyte agonists to regulate the actin polymer network of neutrophils may play an important role in adhesive interactions with the vascular endothelium.