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.

肠道菌群结构和功能的改变被认为在克罗恩氏病（CD）的发病机理中起着重要作用。高通量测序技术的飞速发展导致了与独特的疾病表型和疾病进展实体相关的微生物组风险特征的识别。对已鉴定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。可使用Germfree小鼠模型来研究疾病调节复杂的肠道微生物生态系统（营养不良）或病原体（单一细菌）在CD样炎症的发病机理中的功能。在这里，我们讨论CD背景下gnotobiotic小鼠模型的临床和机制的相关性和局限性。此外，