Ahmed Mohamed, Metwaly Amira, Haller Dirk
Technical University of Munich, Chair of Nutrition and Immunology, School of Life Sciences, 85354 Freising, Germany.
Technical University of Munich, Chair of Nutrition and Immunology, School of Life Sciences, 85354 Freising, Germany; Technical University of Munich, ZIEL Institute for Food & Health, Germany.
Int J Med Microbiol. 2021 Apr;311(3):151489. doi: 10.1016/j.ijmm.2021.151489. Epub 2021 Feb 25.
Alterations in the gut microbiota structure and function are thought to play an important role in the pathogenesis of Crohn's disease (CD). The rapid advancement of high-throughput sequencing technologies led to the identification of microbiome risk signatures associated with distinct disease phenotypes and progressing disease entities. Functional validation of the identified microbiome signatures is essential to understand the underlying mechanisms of microbe-host interactions. Germfree mouse models are available to study the functional role of disease-conditioning complex gut microbial ecosystems (dysbiosis) or pathobionts (single bacteria) in the pathogenesis of CD-like inflammation. Here, we discuss the clinical and mechanistic relevance and limitations of gnotobiotic mouse models in the context of CD. In addition, we will address the role of diet as an essential external factor modulating microbiome changes, potentially underlying disease initiation and development.
肠道微生物群结构和功能的改变被认为在克罗恩病（CD）的发病机制中起重要作用。高通量测序技术的迅速发展使得能够识别与不同疾病表型和疾病进展相关的微生物组风险特征。对已识别的微生物组特征进行功能验证对于理解微生物与宿主相互作用的潜在机制至关重要。无菌小鼠模型可用于研究疾病调节性复杂肠道微生物生态系统（生态失调）或致病共生菌（单一细菌）在类CD样炎症发病机制中的功能作用。在此，我们讨论悉生小鼠模型在CD背景下的临床和机制相关性及局限性。此外，我们将探讨饮食作为调节微生物组变化的重要外部因素的作用，这可能是疾病发生和发展的潜在基础。
