Journal
CIRCULATION RESEARCH
Volume 86, Issue 2, Pages 205-213Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.RES.86.2.205
Keywords
tumor necrosis factor-alpha; hydrogen peroxide; E-selectin; T lymphocyte; neutrophil
Funding
- NIDDK NIH HHS [P01-DK-43785] Funding Source: Medline
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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 AIR-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,im anti-tumor necrosis factor-a 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 H2O2. These findings indicate that H2O2 produced by postanoxic endothelial cells stimulates T cells to produce tumor necrosis factor-alpha, which in turn elicits endothelial cell adhesion molecule expression and a corresponding increase in neutrophil adhesion.
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