T-lymphocyte-derived tumor necrosis factor exacerbates anoxia-reoxygenation-induced neutrophil-endothelial cell adhesion.
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-alpha 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 H(2)O(2). These findings indicate that H(2)O(2) 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.
Kokura
S
S
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
Wolf
R E
RE
Yoshikawa
T
T
Granger
D N
DN
Aw
T Y
TY
D000911:Antibodies, Monoclonal / Q000494:pharmacology; D001381:Azepines / Q000494:pharmacology; D001402:B-Lymphocytes / Q000166:cytology; D002374:Catalase / Q000494:pharmacology; D002448:Cell Adhesion / Q000187:drug effects / Q000276:immunology; D015687:Cell Hypoxia / Q000187:drug effects / Q000276:immunology; D002478:Cells, Cultured; D002860:Chromium Radioisotopes; D019040:E-Selectin / Q000032:analysis / Q000276:immunology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000166:cytology* / Q000276:immunology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D009504:Neutrophils / Q000166:cytology*; D016877:Oxidants / Q000494:pharmacology; D010100:Oxygen / Q000494:pharmacology*; D019007:P-Selectin / Q000032:analysis; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D015427:Reperfusion Injury / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000737:chemistry* / Q000166:cytology / Q000378:metabolism; D014230:Triazoles / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology
D000911:Antibodies, Monoclonal; D001381:Azepines; D002860:Chromium Radioisotopes; D019040:E-Selectin; D016877:Oxidants; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D014230:Triazoles; D014409:Tumor Necrosis Factor-alpha; C052518:WEB 2086; D018799:Intercellular Adhesion Molecule-1; D006861:Hydrogen Peroxide; D002374:Catalase; D010100:Oxygen