| 引用本文： |
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杨行堂,王芝珺,郑佳谊,等.幽门螺杆菌感染的C57BL/6 CD177基因敲除小鼠模型建立[J].同济大学学报（医学版）,2020,41(3):284-290. [点击复制]
- YANG Xing-tang,WANG Zhi-jun,ZHENG Jia-yi,et al.Establishment of CD177 gene knock-out C57BL/6 mouse model infected with Helicobacter pylori[J].同济大学学报（医学版）,2020,41(3):284-290. [点击复制]
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| 摘要: |
| 目的建立幽门螺杆菌（Helicobacter pylori, Hp）感染的C57BL/6 CD177基因敲除（CD177 gene knock-out, CD177 KO）小鼠模型，为进一步进行相关研究奠定基础。方法屏障环境中饲养的无特定病原生物（specific pathogen free, SPF）C57BL/6野生型（wild type, WT）小鼠及CD177基因敲除小鼠各22只，雌雄各半，野生型及CD177基因敲除小鼠各自随机分成2组: 野生型小鼠Hp悉尼菌株（SS1）灌胃组（HpSS1 WT组）10只、野生型小鼠Hp49503株灌胃组（Hp49503 WT组）10只、CD177基因敲除小鼠Hp悉尼株灌胃组（HpSS1 KO组）10只、CD177基因敲除小鼠Hp49503株灌胃组（Hp49503 KO组）10只，另设WT及KO空白对照各1组，各自相应对照组小鼠每组随机各2只，共6组。每组小鼠均禁食12 h后按HpSS1组和Hp49503分组分别予各自菌株的菌液予灌胃。灌胃2周后颈椎脱臼法处死小鼠，取小鼠胃黏膜组织，分别行快速尿素酶实验、病理切片常规H-E染色及特殊组化Warthin-Starry银染色，观察Hp在小鼠胃腔内定植，胃黏膜炎症细胞构成及炎症变化等病理组织学变化情况。结果无论HpSS1株还是Hp49503株在C57BL/6 WT及CD177KO小鼠胃窦隐窝可观察到细菌定植，胃黏膜及胃黏膜下层可见炎症细胞浸润。结论成功建立了Hp感染诱发C57BL/6 CD177KO小鼠胃炎模型。 |
| 关键词: 幽门螺杆菌 CD177 基因敲除 胃炎 模型 |
| DOI：10.16118/j.1008-0392.2020.03.003 |
| 投稿时间：2020-01-07 |
| 基金项目: |
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| Establishment of CD177 gene knock-out C57BL/6 mouse model infected with Helicobacter pylori |
| YANG Xing-tang,WANG Zhi-jun,ZHENG Jia-yi,LIU Zhan-ju |
| (Dept. of Emergency, Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China;Dept. of Pathology, Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China;Dept. of Gastroenterolog, Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China) |
| Abstract: |
| ObjectiveTo establish a C57BL/6 CD177 gene knock out (CD177KO) mouse model infected with Helicobacter pylori (Hp). MethodsTwenty SPF wild type C57BL/6 mice (WT) and 20 SPF CD177 gene knock-out C57BL/6 mice (CD177 KO）were randomly divided into two groups, respectively, with 10 mice in each group. Mice in HpSS1 WT and HpSS1 KO groups were given Hp Sydney Strain 1 (HpSS1, VacA+CagA-) by gavage, while mice in Hp49503 WT and Hp49503 KO groups were given with Hp49503（VacA+CagA+）by gavage. Two WT and a CD177 KO mice were not given Hp and served as control group. Two weeks after treatment the mice were sacrificed, the gastric mucosa samples were taken, and the rapid urease test, routine H-E staining and special histochemical Warthin starry silver staining were performed. The Hp colonization in the gastric cavity, inflammatory cell composition and inflammatory changes of gastric mucosa were observed. ResultsHp colonization was observed in antral crypt of C57BL/6 WT and CD177KO mice infected with HpSS1 or Hp49503, and inflammatory cell infiltration was observed in gastric mucosa and submucosa. ConclusionThe gastritis model of C57BL/6 CD177KO mice induced by Hp infection has been successfully established. |
| Key words: Helicobacter pylori CD177 gene knock-out gastritis model |
