In:
Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 75, No. 2 ( 2004-02-01), p. 286-292
Abstract:
Neutrophils are now considered central to the pathogenesis of most forms of acute lung injury. Neutrophils do not cause damage while suspended in the bloodstream; however, a release of cytotoxic agents occurs when neutrophils are adherent to endothelium, epithelium, or extracellular matrix proteins in the interstitium. Such neutrophil adherence is mediated predominantly through β2 integrins (CD11/CD18) on its surface. This study was undertaken to investigate whether the IκB/nuclear factor (NF)-κB cascade is involved in this β2 integrin-mediated activation of human neutrophils. β2 Integrin Mac-1 (CD11b/CD18) aggregation was induced by antibody cross-linking of the integrins on the cell surface. β2 Integrin aggregation induced interleukin-1β and tumor necrosis factor-α production, which suggests the activation of neutrophils by β2 integrin. IκBα was markedly degraded at 1 h, and NF-κB–DNA-binding activity markedly increased 2 h after β2 integrin aggregation, which activated IκB kinase activity at 1 h. β2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-κB. These findings suggest that the activation of human neutrophils by β2 integrin aggregation is mediated through the activation of the IκB/NF-κB pathway.
Type of Medium:
Online Resource
ISSN:
0741-5400
,
1938-3673
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
2004
detail.hit.zdb_id:
2026833-6
SSG:
12
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