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纸质出版:2009
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陈军华,解元元,朱朝敏,刘作义.轮状病毒感染致乳鼠肠外损害的实验研究[J].陆军军医大学学报(原第三军医大学学报),2009,31(15):1479-1482.
CHEN Jun-hua,XIE Yuan-yuan,ZHU Chao-min,LIU Zuo-yi.Extraintestinal lesions caused by rotavirus: An experimental study on suckling mice[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(15):1479-1482.
目的 探讨轮状病毒(rotavirus
RV)感染引起肠外脏器损害情况及其发病机制。 方法 用MA104细胞培养猴RV SA-11经口感染生后7 d昆明小鼠乳鼠,实验组每只经口接种0.1 ml培养物冻融液(3.75×10
7
pfu/ml),对照组经口接种0.1 ml正常对照细胞冻融液。接种后3 d处死乳鼠,光镜下观察脑、肺、心、肝、胰和肾组织病理改变,电镜下观察心肌细胞超微结构改变;以免疫荧光方法检测各器官RV抗原分布情况;以Phalloidin-TRITC对丝状肌动蛋白染色并经软件(Imageproplus5.1
IPP5.1)测量分析以观察心肌组织丝状肌动蛋白含量有无改变;以原位凋亡细胞检测方法检测肝细胞和心肌细胞凋亡情况;以巢式RT-PCR方法检测各器官内RV RNA分布情况。 结果 在光镜下脑、肺、胰和肾组织未见明显病变,但可见心肌间质水肿,心肌细胞浊肿,肝细胞空泡变性;电镜下心肌细胞肌丝溶解,线粒体内室扩张,滑面内质网扩张,核周间隙增宽;Phalloidin-TRITC染色未见心肌组织丝状肌动蛋白含量改变;除脑组织外其他器官内见到RV抗原分布,而各器官内均有RV-RNA分布;肝细胞凋亡增加,而心肌细胞未见凋亡。 结论 RV可播散到肠外脏器并引起病理损害,但总体上程度较轻。病毒感染导致丝状肌动蛋白解聚及细胞骨架损害、诱导细胞凋亡不仅是肠黏膜损伤的机制,同时也是肠外损害的机制。
Objective To study the extraintestinal lesions induced by rotavirus (RV) infection and explore the pathogenesis. Methods Simian rotavirus SA11 was cultured in MA-104 cells. After inoculation
the pathological changes in brain
lung
heart
liver
pancreas and kidney tissues were observed
the RV antigens detected
and the apoptotic cells observed. Besides
we stained the filamentous actin (F-actin) with Phalloidine-TRITC
and then quantified the F-actin amount. Results Several pathological changes
inclusive of myocardial interstitial edema
granular degeneration in cardiacytes
hepatic congestion
and hepatocellular vacuolar degeneration
were found
but not found in the brain
lung
and pancreas tissues. Meanwhile
several ultrastructural changes
inclusive of dissolved myocardial F-actin
extended smooth endoplasmic reticulum
swollen mitochondria
and widened perinuclear space
were found. No difference was found in the quantity of myocardial F-actin. Apoptosis was found in liver cells
but not in myocardial cells. RV RNA was detected in tissues such as brain
lung
heart
liver and pancreas tissues. Conclusion All the results suggest that RV may spread from the intestine to various extraintestinal organs and hence induce injury. Filamentous actin depolymerization
cytoskeleton damage and apoptosis induced by RV infection are the important mechanism not only in intestinal damages
but also in extraintestinal lesions.
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