Burich A, Hershberg R, Waggie K, Zeng W, Brabb T, Westrich G, Viney J L, Maggio-Price L
Department of Comparative Medicine, University of Washington, Seattle 98195, USA.
Am J Physiol Gastrointest Liver Physiol. 2001 Sep;281(3):G764-78. doi: 10.1152/ajpgi.2001.281.3.G764.
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 wild-type 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 wild-type 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.
炎症性肠病（IBD）被认为是由于对管腔微生物抗原的黏膜免疫反应失调所致，其中T淋巴细胞介导结肠病变。据报道，幽门螺杆菌属感染可在免疫缺陷小鼠中引发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，我们用肝螺杆菌或胆汁螺杆菌感染白细胞介素（IL）-10（-/-）、重组激活基因（Rag）1（-/-）、T细胞受体（TCR）-α（-/-）、TCR-β（-/-）和野生型小鼠，并比较组织病理学IBD表型。IL-10（-/-）小鼠感染胆汁螺杆菌或肝螺杆菌后均出现严重的弥漫性IBD，而Rag1（-/-）、TCR-α（-/-）、TCR-β（-/-）和野生型小鼠对幽门螺杆菌属感染表现出不同的易感性。在感染幽门螺杆菌的患有IBD的IL-10（-/-）和TCR-α（-/-）小鼠的结肠中，促炎细胞因子mRNA表达增加。这些结果证实并扩展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发展中的重要性，但不是严格依赖性。
