Environmental triggers in the context of genetic susceptibility drive phenotypes of complex immune disorders such as Inflammatory bowel disease (IBD). One such trigger of IBD is perturbations in enteric commensal bacteria, fungi or viruses that shape both immune and neuronal state. The epigenome acts as an interface between microbiota and context-specific gene expression and is thus emerging as a third key contributor to IBD. Here we review evidence that the host epigenome plays a significant role in orchestrating the bidirectional crosstalk between mammals and their commensal microorganisms. We discuss disruption of chromatin regulatory regions and epigenetic enzyme mutants as a causative factor in IBD patients and mouse models of intestinal inflammation and consider the possible translation of this knowledge. Furthermore, we present emerging insights into the intricate connection between the microbiome and epigenetic enzyme activity via host or bacterial metabolites and how these interactions fine-tune the microorganism-host relationship.

中文翻译：

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健康和 IBD 中的表观基因组-代谢组-微生物组轴。

遗传易感性背景下的环境触发因素驱动复杂免疫疾病的表型，例如炎症性肠病 (IBD)。IBD 的此类触发因素之一是肠道共生细菌、真菌或病毒的扰动，这些细菌、真菌或病毒塑造了免疫和神经元状态。表观基因组充当微生物群和特定环境基因表达之间的接口，因此正在成为 IBD 的第三个关键贡献者。在这里，我们回顾了宿主表观基因组在协调哺乳动物与其共生微生物之间的双向串扰中发挥重要作用的证据。我们讨论了染色质调控区的破坏和表观遗传酶突变体作为 IBD 患者和小鼠肠道炎症模型的致病因素，并考虑了这些知识的可能转化。此外，