Michael G. DeGroote Institute for Infectious Disease Research, McMaster University, 1200 Main Street West, Hamilton, Ontario, Canada L8N 3Z5.
Nat Commun. 2013;4:1957. doi: 10.1038/ncomms2957.
Crohn's disease is a chronic inflammatory condition of the gastrointestinal tract in which alterations to the bacterial community contribute to disease. Adherent-invasive Escherichia coli are associated with human Crohn's disease; however, their role in intestinal immunopathology is unclear because of the lack of an animal model compatible with chronic timescales. Here we establish chronic adherent-invasive Escherichia coli infection in streptomycin-treated conventional mice (CD1, DBA/2, C3H, 129e and C57BL/6), enabling the study of host response and immunopathology. Adherent-invasive Escherichia coli induces an active T-helper 17 response, heightened levels of proinflammatory cytokines and fibrotic growth factors, with transmural inflammation and fibrosis. Depletion of CD8+ T cells increases caecal bacterial load, pathology and intestinal fibrosis in C57BL/6 mice, suggesting a protective role. Our findings provide evidence that chronic adherent-invasive Escherichia coli infections result in immunopathology similar to that seen in Crohn's disease. With this model, research into the host and bacterial genetics associated with adherent-invasive Escherichia coli-induced disease becomes more widely accessible.
克罗恩病是一种胃肠道的慢性炎症性疾病,其中细菌群落的改变有助于疾病的发生。黏附侵袭性大肠杆菌与人类克罗恩病有关;然而,由于缺乏与慢性时间尺度兼容的动物模型,其在肠道免疫病理学中的作用尚不清楚。在这里,我们在链霉素处理的常规小鼠(CD1、DBA/2、C3H、129e 和 C57BL/6)中建立了慢性黏附侵袭性大肠杆菌感染,从而能够研究宿主反应和免疫病理学。黏附侵袭性大肠杆菌诱导活跃的辅助性 T 细胞 17 反应、促炎细胞因子和纤维化生长因子水平升高,伴有黏膜炎症和纤维化。在 C57BL/6 小鼠中耗尽 CD8+T 细胞会增加盲肠细菌负荷、病理学和肠道纤维化,表明其具有保护作用。我们的研究结果提供了证据,表明慢性黏附侵袭性大肠杆菌感染会导致类似于克罗恩病的免疫病理学。有了这种模型,与黏附侵袭性大肠杆菌诱导的疾病相关的宿主和细菌遗传学的研究变得更加广泛。