Clinical Study On Platelet Microparticle Level In Acute Pancreatitis And Promotion Of Neutrophil Extracellular Traps Formation

Background Acute pancreatitis(AP)is a common clinical acute abdomen.The pathology is pancreatic acinar cell damage mainly,causing trypsinogen activation,which triggers the inflammatory.There is almost mild acute pancreatitis in clinic,but20%-30%of AP patients can develop to severe acute pancreatitis with an increased mortality rate.There are studies shown that neutrophils can activate trypsin to cause pancreatic tissue damage,and platelets have an important role in the process.Platelets activation can form a large number of platelet particles(PMPs),which can promote the recruitment and adhesion of inflammatory cells,releasing proteolytic enzymes and oxygen free radicals,in result of pancreatic parenchymal cells damage.Platelets can induce pancreatic endothelial cells expressing P-selectin,promoting neutrophil activation and mediating platelet-dependent pancreatic tissue infiltration.Regulation of platelet activation and release of PMPs may become a new direction for the treatment of AP.In the study,we investigated the affect of PMPs in the pathogenesis of acute pancreatitis by detecting PMPs stimulating neutrophils to release NETs during acute pancreatitis..Objective To investigate the level of platelet microparticles(PMPs)in acute pancreatitis and the ability of PMPs to promote the formation of neutrophil extracellular traps(NETs).Methods The blood samples of 55 patients with AP admitted to the First Affiliated Hospital of Anhui Medical University from September 2018 to August 2019 were collected,and divided into mild acute pancreatitis(MAP)group(n=26),moderate and severe acute pancreatitis(MSAP)group(n=17)and severe acute pancreatitis(SAP)group(n=12).15 healthy people for physical examination were selected as control group.The platelet poor plasma(PPP)was separated by differential centrifugation and the PMPs were measured by flow cytometry.Neutrophils from control group were collected and co-cultured with PMPs from AP patients.The contents of myeloperoxidase(MPO),neutrophil elastase(NE)and histone H3 were detected by ELISA,and the distribution of NETs was observed by confocal laser scanning microscopy.Results Compared with the control group,the content of PMPs in MAP group,MSAP group and SAP group increased(?~2=50.429,P<0.001).Compared with MAP group and MSAP group,the content of PMPs in SAP group were more(179.50(145.00,308.75)VS 1117.50(483.00,2488.25)VS 1848.00(1216.50,2562.00)/ul,?~2=40.256 P<0.001).The content of PMPs in AP patients was correlated with APACHEII,BISAP and Ranson score(r=0.636,0.508 and 0.430 respectively,P<0.001).Compared with the control group,the levels of MPO(105.27±33.82 vs 374.68±92.01 ng/ml,t=9.105),NE(82.71±19.22 vs 267.45±68.46 ng/ml,t=9.921)and histone H3(4.53±1.48 vs 16.34±4.02 ng/ml,t=7.524)in AP group increased(P<0.001)and the formation of NETs was increased detected by confocal laser scanning microscopy.Conclusion The level of PMPs in AP is significantly increased,which is related to disease activity.PMPs may promote the formation of NETs and aggravate the progression of AP.