Establishment Of Animal Model Of Kawasaki Disease And The Change Of Plasma N-terminal Pro-brain Natriuretic Peptide Levels

ObjectiveKawasaki disease (KD) is a kind of common pediatric autoimmune disease, and it cancause multisystem vasculitis, which is leading to damage in the coronary artery andresulting in serious complications of coronary artery lesions(CAL). So, KD is becomingas the leading cause of acquired heart disease in children of the world．Currently, KDis mainly based on clinical symptoms and ultrasound heartbeat graph to diagnose,lacking of specific biochemical markers for early diagnosis. This article summarizessome methods to establish an animal model of Kawasaki disease, and to measure theblood biochemical indexes, wondering to find a specific index and help the earlydiagnosis of the disease. While the pathogenesis of KD is unknown, the establishmentof the animal model also provides the material basis for the further study.MethodsLactobacillus casei cell wall extract (LCWE) was used for immunization of geneticallypredisposed mice (BALB/C mice) to establish animal model of coronary arteritis. Therewere40mice as experimental group and40mice as control group. Mice（4-6weeksold）were peritoneal injected with0.5ml of NS containing0.5mg LCWE or NS alone for3days, and then8mice in each group were sacrificed on days1,3,5,10and28. Bloodwas collected, and cardiac tissues of mice were removed and preserved in formaldehyde.Then tissue specimens were stained with HE to observe the pathologic changes. After centrifugation, we used the mouse N-terminal pro-brain natriuretic peptide(NT-proBNP) ELASA kit to measure the concentration of NT-proBNP in the plasma.T test was performed on the data obtained, comparing the change of NT-proBNPconcentration between two groups of mice.Results1.After the injection with LCWE, the ratio which BALB/C mice developed histologicalcoronary arteritis of experimental group was77.5%,and that of control group was0.2. In the light microscope, we observed only a little neutrophil accumulation along thevascular endothelium firstly in experimental group mice (day1,3), and then manyneutrophils and lymphocytes infiltration around the vessel wall, accompanied by intimalthickening and a few fibroblasts proliferating on day5.On day10,the inflammatoryresponse involved vascular full-thickness, and we found that arterial muscle and elasticfibers ruptured, following a large number of macrophages infiltration and fibroblastsproliferation. To day28, perivascular inflammatory cells decreased significantly, andappeared fibrous tissue proliferation, leading to arterial stenosis. The control group werenot found corresponding changes in each stage.3. The plasma NT-proBNP concentration of the experimental group was significantlyhigher than that of the control group, and the difference was statistically significant（P＜0.05）. In the experimental group, the concentration of plasma NT-proBNP hasgradually increased in the acute phase of KD (days1~10),and the level decreasedsignificantly on day28. While the level of plasma NT-proBNP had no significantfluctuations in control group of mice.Conclusions1. KD can be induced by immunization of mice with LCWE injected, pathologicalchanges were typical, and the morbidity meets the requirement of research.2. The plasma level of NT-proBNP might be used as a biological index in earlydiagnosis of KD.