摘要
目的研究轮状病毒（RV）感染性腹泻的病理学机制。方法50只3d昆明鼠按接种RV与否随机分为实验组（40只）与对照组（10只），实验组经胃灌入0．2ml（2×10^8 PFU）含病毒（SA11株）培养液，对照组灌人0．2ml不含病毒的培养液，分别于接种后不同时间点观察腹泻情况，ELISA方法检测粪便RV抗原，并取其肠黏膜光镜观察形态学变化及电子显微镜下观察RV定植及细胞超微改变。结果实验组接种病毒后24h均出现腹泻，在接种后4d达高峰，第10天完全恢复正常，粪便ELISA检测RV抗原均为阳性。突出的病理改变为小肠上皮细胞广泛空泡样变性，炎症改变轻微。电镜下绒毛上皮细胞结构完整，紧密连接疏松、增宽，完整性受到破坏。结论猴SA11株可成功感染新生昆明鼠制备RV感染模型。RV腹泻的发生可能是通过破坏肠上皮细胞间连接关系，改变上皮细胞极化，从而影响水电解质平衡；与微绒毛损害、细胞凋亡脱落、绒毛萎缩及隐窝细胞取代关系不大。
Objectives To study the pathological pathogenesis of rotavirus infectious diarrhea. Methods Fifties three-day-old Kunming mice were randomly allocated into experiment group and control group. The mice wereinoculated iutragastrically with an 0.2 ml （2 ×10^8 PFU） of SAIl virus or virus free fluid. Then the diarrhea episode were recorded, virus-shedding were checked by enzyme-linked immunosorbent assay （ELISA） , and the mucous of small intestines were observed under light microscope and electron microscope for confirmation of the adherence of rotavirus and histological and uhramicrostructure changes. Results Diarrhea were developed by 24 hours, peaked by 96 hours and completely recovered after 10 days in experimental group. The obvious pathology of small intestine was extensive vacuolation. However, hyperplasia, necrosis, mucosal thickness and inflammation were slight. The crypt cells were not seen significant changes, their depth was not extended and only slight inflammation was observed. The lesions of ileum were the most prominent. There was a correlation between lesion and diarrhea in terms of diarrhea occurrence and severity. The rotavirus could be seen in the intestinal epithelium, and phagosome, lysosome and mitochondrion swelling also could be seen by electron microscope. There were no obvious structural changes at the villus cells. But the tight junction became broad and its integrity was damaged. Conclusions Neonatal KunMing mice is susceptive to SA11. This model may be suitable for studies of physiological pathogenesis, treatment and vaccine in rotavirus infection. Rotavirus mainly adheres on the matured intestinal villi epithelium.The pathology change is slight. The development of rotavirus diarrhea was related to cell＇ s destroyed connection and altered polarization, but may be not related with the microvilli lesion, apoptosis, atrophy and crypt substitution of cell junctions in the small intestine epithelium.
出处
《临床儿科杂志》
CAS
CSCD
北大核心
2008年第10期862-865,共4页
Journal of Clinical Pediatrics
关键词
轮状病毒
腹泻
新生小鼠
致病机制
rotavirus
diarrhea
neonate mice
pathological pathogenesis
