Infection with Citrobacter rodentium constitutes an attack on the intestinal barrier and results in concerted action by innate and adaptive immune responses to limit bacterial translocation and destroy those bacteria that have breached the intestinal barrier. Among the many immune cell types that are involved in the defence against this infection, Th17 cells as the major producers of the barrier protective cytokine IL-22 during the adaptive phase of the response are most numerous. Their extensive plasticity furthermore results in the production of additional cytokines that previously were ascribed to Th1 cells, such as IFNγ. The timely and coordinated repair of damaged epithelium requires input from environmental factors derived from diet and microbiota metabolism of tryptophan which are transmitted through the aryl hydrocarbon receptor (AHR). Thus, the combination of a robust immune response, coupled with intestinal stem cell differentiation guided by environmental factors, ensures resistance to barrier destruction by intestinal infection.

感染柠檬酸杆菌构成对肠道屏障的攻击，并导致先天性和适应性免疫反应的协同作用，以限制细菌易位并破坏那些已经突破肠道屏障的细菌。在参与防御这种感染的许多免疫细胞类型中，Th17 细胞作为反应的适应性阶段中屏障保护性细胞因子 IL-22 的主要生产者数量最多。此外，它们广泛的可塑性导致产生以前归因于 Th1 细胞的其他细胞因子，例如 IFNγ。受损上皮的及时和协调修复需要来自饮食的环境因素和通过芳烃受体（AHR）传递的色氨酸微生物群代谢的输入。因此，