Keubler Lydia M, Buettner Manuela, Häger Christine, Bleich André
Institute for Laboratory Animal Science, Hannover Medical School, Hannover, Germany.
Inflamm Bowel Dis. 2015 Aug;21(8):1967-75. doi: 10.1097/MIB.0000000000000468.
Complex mechanisms are pulling the strings to initiate the development of inflammatory bowel disease. Current evidence indicates that an interaction of genetic susceptibilities (polymorphisms), environmental factors, and the host microbiota leads to a dysregulation of the mucosal immune system. In the past decades, the interleukin-10-deficient mouse has served as an excellent model to mirror the multifactorial nature of this disease. Here, we want to review in detail the interplay of the genetic factors, immune aspects, and especially summarize and discuss the role of the microbiota contributing to colitis development in the interleukin-10-deficient mouse model of inflammatory bowel disease as a multihit model.
复杂的机制在幕后操纵着炎症性肠病的发生发展。目前的证据表明,遗传易感性(多态性)、环境因素和宿主微生物群之间的相互作用会导致黏膜免疫系统失调。在过去几十年中,白细胞介素-10缺陷小鼠已成为反映该疾病多因素性质的优秀模型。在此,我们想详细回顾遗传因素、免疫方面的相互作用,尤其要总结并讨论在炎症性肠病白细胞介素-10缺陷小鼠多打击模型中,微生物群在结肠炎发展过程中所起的作用。