Helicobacter-induced inflammatory bowel disease in IL-10-and T cell-deficient mice
Helicobacter-induced inflammatory bowel disease in IL-10-and T cell-deficient mice
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DOI：
10.1152/ajpgi.2001.281.3.g764
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发表时间：
2001-09-01
影响因子：
4.5
通讯作者：
Maggio-Price, L
中科院分区：
文献类型：
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作者：
Burich, A;Hershberg, R;Maggio-Price, L
炎症性肠病(IBD)被认为是由于粘膜对管腔微生物抗原的免疫反应失调所致，T淋巴细胞介导了结肠的病理。据报道，感染幽门螺杆菌可导致免疫缺陷小鼠的IBD，其中一些小鼠缺乏T淋巴细胞。为了进一步了解T细胞和微生物抗原在引发IBD中的作用，我们用白介素10(-/-)、重组酶激活基因(RAG)1(-/-)、T细胞受体(TCR)-α(-/-)、TCR-β(-/-)和野生型小鼠感染肝螺杆菌和胆汁螺杆菌，并比较了IBD的组织病理学表型。IL-10(-/-)小鼠表现为严重弥漫性IBD合并胆汁螺杆菌或H型肝炎，而Rag1(-/-)、TCR-α(-/-)、TCR-β-/-和野生型小鼠对螺杆菌感染表现出不同的易感性。幽门螺杆菌感染IL-10(-/-)和TCR-α(-/-)IBD小鼠结肠促炎症细胞因子mRNA表达增加。这些结果证实并扩大了幽门螺杆菌作为研究微生物诱导的IBD的有用工具的作用，并表明T细胞在细菌诱导的IBD的发展中的重要性，但并不是严格的依赖。
Inflammatory bowel disease (IBD) is thought to result from a dysregulated mucosal immune response to luminal microbial antigens, with T lymphocytes mediating the colonic pathology. Infection with Helicobacter spp has been reported to cause IBD in immunodeficient mice, some of which lack T lymphocytes. To further understand the role of T cells and microbial antigens in triggering IBD, we infected interleukin (IL)-10(-/-), recombinase-activating gene (Rag)1(-/-), T-cell receptor (TCR)-alpha (-/-), TCR-beta (-/-), and wildtype mice with Helicobacter hepaticus or Helicobacter bilis and compared the histopathological IBD phenotype. IL-10(-/-) mice developed severe diffuse IBD with either H. bilis or H. hepaticus, whereas Rag1(-/-), TCR-alpha (-/-), TCR-beta-/-, and wildtype mice showed different susceptibilities to Helicobacter spp infection. Proinflammatory cytokine mRNA expression was increased in the colons of Helicobacter-infected IL-10(-/-) and TCR-alpha (-/-) mice with IBD. These results confirm and extend the role of Helicobacter as a useful tool for investigating microbial-induced IBD and show the importance, but not strict dependence, of T cells in the development of bacterial-induced IBD.