We tested the effect of urinary TNF-binding protein (uTBP) on the toxic effect of TNF (0.5 micrograms/mouse, i.v.) in adrenalectomized mice sensitized with IL-1 to increase susceptibility to TNF. In this experimental model, mortality was 67%, but decreased to 13% when uTBP (250 micrograms/mouse, i.v.) was administered simultaneously with TNF. The protective effect of uTBP was dose-dependent, and time course experiments indicated a protective effect when uTBP was administered before or up to one hour after TNF. Some protection was also obtained when uTBP was given three hours after TNF. Urinary TBP improved the survival of mice after a lethal dose of LPS (1.2 mg/mouse, i.p.), suggesting its possible efficacy in the therapy of septic shock or other TNF-mediated pathologies.
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Cells
October 2024
Clinic of Nephrology, Hypertension, Diabetes and Endocrinology, Otto-von-Guericke University Magdeburg, 39120 Magdeburg, Germany.
DNA-binding protein A (DbpA) belongs to the Y-box family of cold shock domain (CSD) proteins that bind RNA/DNA and exert intracellular functions in cell stress, proliferation, and differentiation. Given the pattern of DbpA staining in inflammatory glomerular diseases, without adherence to cell boundaries, we hypothesized extracellular protein occurrence and specific functions. Lipopolysaccharide and ionomycin induce DbpA expression and secretion from melanoma and mesangial cells.
View Article and Find Full Text PDFObjective: To investigate the effect of mutations in the tumor necrosis factor receptor superfamily 1A (TNFRSF1A) gene on the conformation and behavior of the TNFRSF1A protein. Mutations in TNFRSF1A cause the autosomal-dominant, autoinflammatory TNFR-associated periodic syndrome (TRAPS).
Methods: The expression of recombinant TNFRSF1A was compared in SK-HEp-1 endothelial cells and HEK 293 epithelial cells stably transfected with full-length R347A or Deltasig constructs of wild-type or TRAPS-associated mutant TNFRSF1A.
Am J Physiol Heart Circ Physiol
February 2002
Department of Urology, Johns Hopkins University, Baltimore, Maryland 21287, USA.
While tumor necrosis factor (TNF)-alpha is an important mediator of renal ischemia-reperfusion (I/R) injury, its role in contralateral renal injury after isolated renal ischemia remains unknown. We therefore investigated the effect of isolated left renal ischemia on the nonischemic contralateral kidney. To study this, male Sprague-Dawley rats were anesthetized and exposed to varying degrees of left renal I/R injury.
View Article and Find Full Text PDFAm J Physiol Regul Integr Comp Physiol
January 2002
Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.
The purpose of the present study was to determine whether burn-induced changes in various components of the insulin-like growth factor (IGF) system are mediated by the actions of endogenous glucocorticoids or tumor necrosis factor (TNF). To address this aim, a 30% total body surface area full-thickness scald burn was produced in anesthetized rats, and the animals were studied 24 h later. Separate groups of time-matched control and burned rats were pretreated with either an antagonist to glucocorticoids (RU-486) or to TNF (TNF-binding protein; TNFBP).
View Article and Find Full Text PDFViral Immunol
November 1999
The University of Regensburg, Department of Medicine I, Germany.
Freshly isolated macrophages from mature mice are poorly or nonpermissive for infections with HSV. However, despite lack of significant viral replication, HSV infection has been demonstrated to induce substantial cell death among macrophages. To determine if HSV-induced cytotoxicity of macrophages is due to apoptosis, peritoneal macrophages were obtained from C57BL/6 (B6) mice, and apoptosis was analyzed following HSV-2 infection in vitro.
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