Abstract
Extracellular heat shock proteins (HSPs) mediate immunological functions and are involved in pathologies such as infection, stress, and cancer. Here, we demonstrated the dependence of an amount of HSP70 and HSP90 in serum vs. severity of acute pancreatitis (AP) on a cohort of 49 patients. Tethered bilayer lipid membranes (tBLMs) have been developed to investigate HSPs’ interactions with tBLMs that can be probed by electrochemical impedance spectroscopy (EIS). The results revealed that HSP70 and HSP90 interact via different mechanisms. HSP70 shows the damage of the membrane, while HSP90 increases the insulation properties of tBLM. These findings provide evidence that EIS offers a novel approach for the study of the changes in membrane integrity induced by HSPs proteins. Herein, we present an alternative electrochemical technique, without any immunoprobes, that allows for the monitoring of HSPs on nanoscaled tBLM arrangement in biologics samples such us human urine. This study demonstrates the great potential of tBLM to be used as a membrane based biosensor for novel, simple, and non-invasive label-free analytical system for the prediction of AP severity.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
Aiming to determine the prognostic utility of serum heat shock proteins (HSPs) for evaluation of severity level in the early assessment of acute pancreatitis (AP) clinical course, a cohort consisting of control (C), mild (M), moderately severe (MS), or severe (S) patients has been assessed
The severity of AP was evaluated by clinical examination, laboratory and radiological tests methodology and the concentrations of HSP70 and HSP90 in serum were detected by enzyme-linked immunosorbent assay (ELISA) assessments
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. M in AP progress is the most frequent (80%), and usually self-limiting, but around 20% go on to develop MS or S forms that involve pancreatic or peri-pancreatic tissue necrosis and/or organ failure. Mortality in those that develop sterile necrosis of the pancreas is reported to be 13% and, if there is infection, mortality can increase to up to 35% [2]. Many etiological factors are involved in the pathogenesis of AP, and its mechanisms should be studied
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