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非洲猪瘟病毒致心脏损伤的病理学观察及其损伤机制研究 被引量:1

Pathological observation of cardiac injury caused by African swine fever virus infection and the study on its injury mechanism
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摘要 为了进一步探讨急性非洲猪瘟(African swine fever,ASF)对心脏组织的损伤机制,试验将18头健康长白猪随机分为2组,其中攻毒组(13头)采用肌肉注射方式注射Ⅱ型非洲猪瘟病毒(African swine fever virus,ASFV)毒株Pig/HLJ/18(1×10^(2)HAD_(50)/mL),剂量为5 mL/头,对照组(5头)采用相同方式注射相同体积的生理盐水。试验期间观察试验猪的临床表现,解剖所有试验猪并采集心脏组织,观察剖检变化及组织学病变;采用免疫组织化学方法对肿瘤坏死因子-α(TNF-α)、γ干扰素(IFN-γ)、白细胞介素-1β(IL-1β)及细胞间黏附分子-1(ICAM-1)、血小板内皮黏附分子-1(CD31)的表达情况进行检测。结果表明:攻毒组的发病率和死亡率均为100%,发病猪体温升高、食欲减退、呼吸困难,剖检可见攻毒组心外膜与心内膜有点状或灶状出血,随着病程延长出血加重并出现淡黄色或黄红色心包积液,少数死亡猪出现出血性纤维素渗出;组织学病变观察以心肌缺血及血管损伤为主要病理变化,心肌纤维可见肿胀、断裂,心肌间质增宽,心肌间质血管有明显充血和出血,周围有大量淋巴细胞浸润,血管内皮细胞肿胀、坏死、脱落。攻毒组炎性因子TNF-α、IL-1β与IFN-γ主要存在于心肌细胞与血管内皮细胞中,且阳性细胞表达率极显著高于对照组(P<0.01);黏附分子ICAM-1主要存在于血管内皮细胞中,且阳性细胞表达率极显著高于对照组(P<0.01),而CD31阳性细胞表达率极显著低于对照组(P<0.01)。说明感染Ⅱ型ASFV后心脏组织产生并释放大量炎性因子,使血管内皮细胞的完整性受损,血管的通透性增加,从而造成明显的心脏组织损伤。 In order to further investigate the cardiac injury caused by acute African swine fever(ASF),in this experiment,18 healthy Long White pigs were randomly divided into 2 groups;the challenge group(13 heads)was injected with typeⅡAfrican swine fever virus(ASFV)strain Pig/HLJ/18 by intramuscular injection at a dose of 1×10^(2)HAD_(50)/mL,and the control group(5 heads)was injected with the same dose of normal saline.During the experiment,the clinical symptoms of the test pigs were observed;all the test pigs were dissected and heart tissues were collected,and the autopsy changes and histological lesions were observed.The expressions of tumour necrosis factor-α(TNF-α),γinterferon(IFN-γ),interleukin-1β(IL-1β),intercellular adhesion molecule-1(ICAM-1)and platelet endothelial cell adhesion molecule-1(CD31)were detected by immunohistochemistry method.The results showed that the morbidity and mortality of the Long White pigs in the challenge group were 100%.The affected pigs had increased body temperature,loss of appetite and difficult breathing.The autopsy showed that the epicardium and endocardium in the challenge group were point-like or focal hemorrhage and the bleeding worsened with the prolongation of the disease;yellowish or yellow-red pericardial effusion appeared;a small number of dead pigs showed hemorrhagic cellulose exudation.Histological observation showed myocardial ischemia and vascular damage as the main pathological changes;myocardial fibers might be swollen,ruptured,and myocardial interstitial widening;myocardial interstitial vessels showed massive hyperemia and hemorrhage,surrounded by a large number of lymphocytic infiltration;vascular endothelial cells were accompanied by swelling,necrosis,and exfoliation.The inflammatory factors TNF-α,IL-1βand IFN-γin the challenge group were mainly present in cardiomyocytes and vascular endothelial cells,and the expression rates in positive cells were significantly higher than those in the control group(P<0.01).The adhesion molecule ICAM-1 in the challenge group was mainly present in vascular endothelial cells,and the expression rate in positive cells was significantly higher than that in the control group(P<0.01),while the expression rate of CD31 in positive cells was significantly lower than that in the control group(P<0.01).The results suggested that after infection with type II ASFV,heart tissue produced and released a large number of inflammatory factors,which impaired the integrity of vascular endothelial cells and increased the permeability of blood vessels,resulting in obvious cardiac injury.
作者 付静静 刘伟琪 李慧 罗颖 张先东 许正涛 李樵锋 邓桦 黄璐琦 杨鸿 FU Jingjing;LIU Weiqi;LI Hui;LUO Ying;ZHANG Xiandong;XU Zhengtao;LI Qiaofeng;DENG Hua;HUANG Luqi;YANG Hong(School of Life Science and Engineering,Foshan University,Foshan 528231,China;China Academy of Chinese Medical Sciences,Beijing 100193,China)
出处 《黑龙江畜牧兽医》 北大核心 2023年第13期1-4,130,131,共6页 Heilongjiang Animal Science And veterinary Medicine
基金 中央本级重大增减支项目(2060302)。
关键词 非洲猪瘟 心脏损伤 病理变化 炎性因子 细胞间黏附分子-1 血小板内皮黏附分子-1 African swine fever cardiac injury pathological changes inflammatory factors intercellular adhesion molecule-1 platelet endothelial cell adhesion molecule-1
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