Soluble receptors released during acute pancreatitis interfere with the detection of tumor necrosis factor-α
- 1 May 2001
- journal article
- laboratory investigations
- Published by Wolters Kluwer Health in Critical Care Medicine
- Vol. 29 (5), 1023-1026
- https://doi.org/10.1097/00003246-200105000-00029
Abstract
To evaluate the interfering effect of tumor necrosis factor-alpha soluble receptor when measuring circulating concentrations of tumor necrosis factor-alpha in an experimental model of acute pancreatitis. Randomized, controlled trial. Experimental laboratory. Male Wistar rats. Acute pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Saline was administered in a control group. Serums were overloaded with known amounts of tumor necrosis factor-alpha or macrophage inflammatory protein-2. Three hours after induction, serum concentrations of free tumor necrosis factor-alpha, total tumor necrosis factor-alpha, and soluble receptor of tumor necrosis factor-alpha were measured. No detectable concentrations of free tumor necrosis factor-alpha were found in any experimental group. By contrast, significant increases in total tumor necrosis factor-alpha and soluble receptor of tumor necrosis factor-alpha were found after induction of pancreatitis. Overloading of serum with tumor necrosis factor-alpha resulted in detection of 50% of the expected concentrations of free tumor necrosis factor-alpha from control animals and only of 5% from the pancreatitis group. Overloading the serum with macrophage inflammatory protein-2 resulted in a detection of 100% of the expected concentrations in both control and treated animals. Circulating soluble receptor of tumor necrosis factor-alpha could interfere with the detection of tumor necrosis factor-alpha in some pathologies, such as pancreatitis, that are associated with increases in soluble receptor of tumor necrosis factor-alpha.Keywords
This publication has 15 references indexed in Scilit:
- Activation of Alveolar Macrophages in Lung Injury Associated With Experimental Acute Pancreatitis Is Mediated by the LiverAnnals of Surgery, 1999
- Leukotriene generation and neutrophil infiltration after experimental acute pancreatitis.Inflammation, 1998
- Serum concentrations of inflammatory mediators related to organ failure in patients with acute pancreatitisBritish Journal of Surgery, 1996
- Circulating Endotoxin, Tumour Necrosis Factor-Alpha, and Their Natural Antagonists in the Pathophysiology of Acute PancreatitisScandinavian Journal of Gastroenterology, 1996
- Acute Pancreatitis Induces Intrapancreatic Tumor Necrosis Factor Gene ExpressionArchives of Surgery, 1995
- Induction of acute pancreatitis in germ-free rats: Evidence of a primary role for tumor necrosis factor-alphaSurgery, 1995
- Soluble receptors for tumour necrosis factor in clinical laboratory diagnosisEuropean Journal of Haematology, 1995
- Role of tumor necrosis factor-α in disease states and inflammationCritical Care Medicine, 1993
- Two TNF receptorsImmunology Today, 1992
- Experimental pancreatitis in the rat. — Ductal factors in sodium taurocholate-induced acute pancreatitisExperimental pathology, 1984