The aryl hydrocarbon receptor (AHR) is widely expressed in immune and non-immune cells of the gut and its activation has been correlated to the outcome of inflammatory bowel diseases (IBD). In ulcerative colitis and Crohn’s disease, there is an excessive chronic inflammation with massive accumulation of leukocytes in the gut, in an attempt to constrain the invasion of pathogenic microorganisms on the damaged organ. Accordingly, it is known that dietary components, xenobiotics, and some chemicals or metabolites can activate AHR and induce the modulation of inflammatory responses. In fact, the AHR triggering by specific ligands during inflammatory conditions results in decreased IFNγ, IL-6, IL-12, TNF, IL-7, and IL-17, along with reduced microbial translocation and fibrosis in the gut. Moreover, upon AHR activation, there are increased regulatory mechanisms such as IL-10, IL-22, prostaglandin E₂, and Foxp3, besides the production of anti-microbial peptides and epithelial repair. Most interestingly, commensal bacteria or their metabolites may also activate this receptor, thus contributing to the restoration of gut normobiosis and homeostasis. In line with that, Lactobacillus reuteri, Lactobacillus bulgaricus, or microbial products such as tryptophan metabolites, indole-3-pyruvic acid, urolithin A, short-chain fatty acids, dihydroxyquinoline, and others may regulate the inflammation by mechanisms dependent on AHR activation. Hence, here we discussed the potential modulatory role of AHR on intestinal inflammation, focused on the reestablishment of homeostasis through the receptor triggering by microbial metabolites. Finally, the development of AHR-based therapies derived from bacteria products could represent an important future alternative for controlling IBD.

芳烃受体 (AHR) 在肠道的免疫和非免疫细胞中广泛表达，其激活与炎症性肠病 (IBD) 的结果相关。在溃疡性结肠炎和克罗恩病中，存在过度的慢性炎症，白细胞在肠道内大量积聚，试图限制病原微生物对受损器官的侵袭。因此，众所周知，膳食成分、异生物质和一些化学物质或代谢物可以激活 AHR 并诱导炎症反应的调节。事实上，在炎症条件下由特定配体触发的 AHR 导致 IFNγ、IL-6、IL-12、TNF、IL-7 和 IL-17 减少，同时肠道中微生物易位和纤维化减少。此外，在 AHR 激活后，₂和 Foxp3，除了产生抗微生物肽和上皮修复。最有趣的是，共生细菌或其代谢物也可能激活该受体，从而有助于恢复肠道正常生态和体内平衡。与此一致的是，罗伊氏乳杆菌、保加利亚乳杆菌或微生物产物，如色氨酸代谢物、吲哚-3-丙酮酸、尿石素 A、短链脂肪酸、二羟基喹啉等，可能通过依赖于 AHR 激活的机制来调节炎症。因此，我们在这里讨论了 AHR 对肠道炎症的潜在调节作用，重点是通过微生物代谢物触发的受体重建体内平衡。最后，开发源自细菌产品的基于 AHR 的疗法可能代表未来控制 IBD 的重要替代方案。