肠炎沙门菌(Salmonella enteritidis,SE)是引起人类食源性疾病的重要革兰阴性菌之一,可引起禽、家畜等动物较为严重的感染症状。本研究为了建立肠炎沙门菌感染ICR小鼠模型,标准菌株SE 50336分别以1×10~8、1×10~7、1×0~6、1×10~5、1×10~4CFU/mL的剂量通过口腔灌注方式感染6周龄ICR雌鼠,每组10只,以接种PBS的10只小鼠作为对照组,测定肠炎沙门菌对ICR小鼠的半数致死量(LD_(50))。将40只ICR雌鼠随机分成两组,以测定的LD_(50)剂量接种肠炎沙门菌,通过临床症状、体重变化、组织病理学、组织中细菌载量以及TNF-α与IL-6表达水平评价肠炎沙门菌对小鼠的致病性。结果,标准菌株SE 50336对ICR小鼠的LD_(50)为1×10~(5.67)CFU/mL。感染后第3天,小鼠出现采食量下降、活动减少、皮毛色泽变暗、畏寒扎堆等症状;感染后第5天,小鼠的平均体重较对照组呈现下降趋势,后期开始恢复。组织病理学结果显示,肝脏出现灶状坏死,形成血栓,出现坏死细胞;脾脏先后出现纤维素性坏死性脾炎,白髓内淋巴细胞减少,呈小空泡状,出现坏死灶。菌落载量分析发现,细菌载量随着感染进程而升高,在脾脏中繁殖速度最快,载量也最高,肝脏次之。定量PCR结果显示,TNF-α表达水平呈升高趋势,而IL-6表达水平降低。上述结果表明,本试验成功建立了肠炎沙门菌标准菌株SE50336感染ICR小鼠的模型,为肠炎沙门菌感染与致病机制的研究提供了有价值的动物模型,也为表达抗菌肽转基因小鼠抗肠炎沙门菌的评价奠定了基础。 Salmonella enteritidis (SE) is one of the most important Gram-negative bacteria that cause food-borne diseases in human. It can cause severe infection in animals such as poultry and livestock. In this study, in order to establish an ICR mouse model of Salmonella enteritidis infection, the standard strain SE 50336 was treated with 1 × 10-8, 1 × 10-7, 1 × 0-6, 1 × 10-5, 1 × 10-4CFU / mL (IC50) mice were inoculated intraperitoneally with ICR mice of 6 weeks old by intraperitoneal injection, with 10 mice in each group. Ten mice inoculated with PBS were used as control group. The median lethal dose (LD 50) of Salmonella enteritidis in ICR mice was determined. Forty ICR female mice were randomly divided into two groups and inoculated with Salmonella enteritidis at the determined LD50 dose. The clinical symptoms, body weight changes, histopathology, bacterial load in tissues and the expression of TNF-α and IL-6 To evaluate the pathogenicity of S. Enteritidis in mice. As a result, the standard strain SE 50336 had LD 50 of 1 × 10 ~ (5.67) CFU / mL for ICR mice. On the third day after infection, the mice showed decreased feed intake, reduced activity, darker fur coat, and chills and other symptoms. On the fifth day after infection, the average body weight of mice showed a downward trend compared with that of the control group and recovered at the later stage. Histopathological results showed that the liver appeared focal necrosis, the formation of thrombus, necrosis cells; spleen has cellulite necrotic splenitis, white blood within the lymphocytes decreased, small vacuoles, necrosis. Colonies load analysis found that bacterial load increased with the progress of infection, spleen in the fastest breeding speed, the highest load, followed by the liver. Quantitative PCR results showed that TNF-α expression levels increased, while IL-6 expression levels decreased. The above results show that this experiment successfully established a model of S. Enteritidis strain SE50336 ICR mice infected with Salmonella enteritidis infection and pathogenic mechanism of the study provides a valuable animal model, but also for the expression of antimicrobial peptide transgenic mouse anti Enteritis Salmonella evaluation laid the foundation.