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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Escherichia coli infection induces autoimmune cholangitis and anti-mitochondrial antibodies in non-obese diabetic (NOD).B6 (Idd10/Idd18) mice
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Escherichia coli infection induces autoimmune cholangitis and anti-mitochondrial antibodies in non-obese diabetic (NOD).B6 (Idd10/Idd18) mice

机译：大肠杆菌感染在非肥胖糖尿病（NOD）.B6（Idd10 / Idd18）小鼠中诱发自身免疫性胆管炎和抗线粒体抗体

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Summary: Several epidemiological studies have demonstrated that patients with primary biliary cirrhosis (PBC) have a higher incidence of urinary tract infections (UTI) and there is significant homology of the immunodominant mitochondrial autoantigen, the E2 component of the pyruvate dehydrogenase complex (PDC-E2), between mammals and bacteria. Previous work has demonstrated that non-obese diabetic (NOD).B6 Idd10/Idd18 infected with Novosphingobium aromaticivorans developed liver lesions similar to human PBC. It was postulated that the biliary disease was dependent upon the presence of the unique N.aro glycosphingolipids in activating natural killer T (NKT) cells. To address this issue, we infected NOD.B6 Idd10/Idd18 mice with either Escherichia coli, N.aro or use of a phosphate-buffered saline (PBS) vehicle control and serially followed animals for the appearance of liver pathology and anti-mitochondrial autoantibodies (AMA). Of striking importance, the biliary disease of E.coli-infected mice was more severe than N. Aro-infected mice and the titre of AMA was higher in E.coli-infected mice. Furthermore, the immunopathology did not correlate with the ability of bacterial extracts to produce antigen-dependent activation of NKT cells. Our data suggest that the unique glycosphingolipids of N.aro are not required for the development of autoimmune cholangitis. Importantly, the data highlight the clinical significance of E.coli infection in a genetically susceptible host, and we suggest that the appearance of autoimmune cholangitis is dependent upon molecular mimicry. These data highlight that breach of tolerance to PDC-E2 is probably the first event in the natural history of PBC in genetically susceptible hosts.
机译：摘要：几项流行病学研究表明，原发性胆汁性肝硬化（PBC）患者的尿路感染（UTI）发病率较高，并且免疫优势线粒体自身抗原与丙酮酸脱氢酶复合物（PDC-E2 ），介于哺乳动物和细菌之间。先前的研究表明，非肥胖糖尿病（NOD）。感染了新孢子虫芳香族人的B6 Idd10 / Idd18会产生类似于人PBC的肝脏病变。据推测，胆道疾病取决于活化自然杀伤T（NKT）细胞中独特的N.aro糖鞘脂的存在。为了解决此问题，我们用大肠杆菌，N.aro或磷酸盐缓冲液（PBS）载体对照感染了NOD.B6 Idd10 / Idd18小鼠，并连续跟踪动物的肝脏病理学和抗线粒体自身抗体（AMA）。极为重要的是，大肠杆菌感染的小鼠的胆道疾病比N. Aro感染的小鼠更为严重，而大肠杆菌感染的小鼠的滴度更高。此外，免疫病理学与细菌提取物产生依赖抗原的NKT细胞活化能力无关。我们的数据表明，N.aro独特的鞘糖脂对于自身免疫性胆管炎的形成不是必需的。重要的是，这些数据突出了在遗传易感宿主中大肠杆菌感染的临床意义，并且我们建议自身免疫性胆管炎的出现取决于分子模拟。这些数据表明，对PDC-E2的耐受性破坏可能是遗传易感宿主中PBC自然史上的第一件事。

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