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(Circulation Research. 2000;86:205.)
© 2000 American Heart Association, Inc.

Cellular Biology

T-Lymphocyte–Derived Tumor Necrosis Factor Exacerbates Anoxia-Reoxygenation–Induced Neutrophil–Endothelial Cell Adhesion

Satoshi Kokura, Robert E. Wolf, Toshikazu Yoshikawa, D. Neil Granger, Tak Yee Aw

From the Department of Molecular and Cellular Physiology (S.K., D.N.G., T.Y.A.) and the Center of Excellence in Arthritis and Rheumatism (R.E.W.), Louisiana State University Medical Center, Shreveport, and the First Department of Internal Medicine (T.Y.), Kyoto Prefectural University of Medicine, Kyoto, Japan.

Correspondence to Tak Yee Aw, PhD, Department of Molecular and Cellular Physiology, LSU Medical Center, 1501 Kings Highway, Shreveport, LA 71130-3932. E-mail taw{at}lsumc.edu

Abstract—The overall objective of this study was to determine whether T lymphocytes can modulate the increased neutrophil adherence and upregulation of endothelial cell adhesion molecules in human umbilical vein endothelial cells (HUVECs) exposed to anoxia/reoxygenation (A/R). HUVEC monolayers were exposed to 60 minutes of anoxia, followed by 4 hours of reoxygenation in the absence or presence of human T lymphocytes. The A/R-induced neutrophil adhesion was significantly enhanced when T lymphocytes and HUVECs were cocultured for the first 45 minutes of reoxygenation. This was accompanied by a more pronounced increase in E-selectin expression. When T lymphocytes were cocultured with HUVECs by use of inserts that prevented direct cell-cell contact, a comparable A/R-induced enhancement of neutrophil adhesion and of E-selectin expression was observed, indicating that soluble factors produced by T lymphocytes mediate the exaggerated A/R-induced inflammatory responses. Treatment with either an anti–tumor necrosis factor- antibody or catalase attenuated the T-cell–mediated responses in postanoxic HUVECs. Moreover, the T-cell–mediated neutrophil adhesion response was mimicked by exposure of naive HUVECs to H₂O_2. These findings indicate that H₂O₂ produced by postanoxic endothelial cells stimulates T cells to produce tumor necrosis factor-, which in turn elicits endothelial cell adhesion molecule expression and a corresponding increase in neutrophil adhesion.

Key Words: tumor necrosis factor- • hydrogen peroxide • E-selectin • T lymphocyte • neutrophil

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