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Soluble receptors released during acute pancreatitis interfere with the detection of tumor necrosis factor-alpha
E Folch1, A Serrano, L Sabater
1Department of Medical Bioanalysis, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas-Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
Objective:
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.
Design:
Randomized, controlled trial.
Setting:
Experimental laboratory.
Subjects:
Male Wistar rats.
Interventions:
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.
Measurements And Main Results:
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.
Conclusion:
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.