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目的 胃肠感染是大多数动物类传染性海绵状脑病(TSE)传播的最主要途径。建立羊瘙痒因子263K灌胃感染仓鼠动物模型,并研究其发病特征。方法 Scrapie 263K毒株低剂量和高剂量经灌胃途径接种金黄仓鼠,在终末期取脑组织,用HE染色观察病理变化,免疫组化法检测PrPSc 的组织沉积特点, Western blot 检测PrPSc 分子特征。结果 低剂量灌胃组仅一只动物发病,高剂量组所有接种动物均发病,潜伏期较颅内注射组明显延长。在脑组织中观察到典型的病理改变;PrPSc免疫组化检测显示弥漫性沉积于脑组织,主要累及脑干、大脑皮层深层、小脑,基本与病理学改变累及的区域一致;Western Blot检测发现感染动物脑提取物出现可抵抗蛋白酶消化的PrPSc条带,与颅内注射组脑组织提取物中PrPSc电泳性状完全一致。结论 羊瘙痒因子263K灌胃可成功引起动物发病,与颅内注射比较,潜伏期、神经病理变化和PrPsc沉积均有不同,可能受到感染途径的影响。
Purpose Gastrointestinal infections are the most common route of transmission of most animal transmissible spongiform encephalopathies (TSE). The animal model of hamster infected with pruritus factor 263K was established, and its onset characteristics were studied. Methods The low dose and high dose of Scrapie 263K strain were inoculated with golden hamster via intragastric route. The brain tissues were harvested at the end of the experiment. The pathological changes were observed by HE staining. The characteristics of PrPSc were detected by immunohistochemistry and the molecular characteristics of PrPSc by Western blot. Results Only one animal in the low-dose gavage group developed disease. All the vaccinated animals in the high-dose group developed symptoms, and the incubation period was significantly longer than that in the intracranial injection group. Typical pathological changes were observed in brain tissue. PrPSc immunohistochemistry showed diffuse deposition in brain tissue, mainly involving the brain stem, deep cerebral cortex and cerebellum, which were basically consistent with the pathological changes. Western Blot showed that the infection PrPSc bands in animal brain extracts that could resist protease digestion were completely consistent with the PrPSc electrophoresis traits in intracerebral injection brain tissue extracts. Conclusion The pruritus factor 263K can induce the onset of the disease successfully. Compared with intracranial injection, the latency, neuropathological changes and PrPsc deposition are different, which may be affected by the route of infection.