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Published online before print October 23, 2003
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B/NF-B pathway
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University College of Medicine; Clinical Research Institute, Seoul National University Hospital; and Lung Institute, Medical Research Center, Seoul National University, Korea
2 Correspondence: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National University Hospital, 28 Yongon-dong, Chongno-gu, Seoul 110-744, Korea. E-mail: cgyoo{at}snu.ac.kr
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 ß2 integrins (CD11/CD18) on its surface. This study was undertaken to investigate whether the I
B/nuclear factor (NF)-B cascade is involved in this ß2 integrin-mediated activation of human neutrophils. ß2 Integrin Mac-1 (CD11b/CD18) aggregation was induced by antibody cross-linking of the integrins on the cell surface. ß2 Integrin aggregation induced interleukin-1ß and tumor necrosis factor-
production, which suggests the activation of neutrophils by ß2 integrin. IB was markedly degraded at 1 h, and NF-B–DNA-binding activity markedly increased 2 h after ß2 integrin aggregation, which activated IB kinase activity at 1 h. ß2 Integrin-induced cytokine production was suppressed by MG132 or SN50 pretreatment, which blocked the activation of NF-B. These findings suggest that the activation of human neutrophils by ß2 integrin aggregation is mediated through the activation of the IB/NF-B pathway.
Key Words: adhesion • acute lung injury • CD11b/CD18 • IL-1ß • TNF-
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