Dynamic interactions between gut microbiota and a host’s innate and adaptive immune systems play key roles in maintaining intestinal homeostasis and inhibiting inflammation. The gut microbiota metabolizes proteins and complex carbohydrates, synthesize vitamins, and produce an enormous number of metabolic products that can mediate cross-talk between gut epithelial and immune cells. As a defense mechanism, gut epithelial cells produce a mucosal barrier to segregate microbiota from host immune cells and reduce intestinal permeability. An impaired interaction between gut microbiota and the mucosal immune system can lead to an increased abundance of potentially pathogenic gram-negative bacteria and their associated metabolic changes, disrupting the epithelial barrier and increasing susceptibility to infections. Gut dysbiosis, or negative alterations in gut microbial composition, can also dysregulate immune responses, causing inflammation, oxidative stress, and insulin resistance. Over time, chronic dysbiosis and the translocation of bacteria and their metabolic products across the mucosal barrier may increase prevalence of type 2 diabetes, cardiovascular disease, inflammatory bowel disease, autoimmune disease, and a variety of cancers. In this paper, we highlight the pivotal role gut microbiota and their metabolites (short-chain fatty acids (SCFAs)) play in mucosal immunity.

中文翻译：

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肠道菌群与免疫系统的相互作用

肠道菌群与宿主先天性和适应性免疫系统之间的动态相互作用在维持肠道动态平衡和抑制炎症中起着关键作用。肠道菌群代谢蛋白质和复杂的碳水化合物，合成维生素，并产生大量的代谢产物，可以介导肠道上皮与免疫细胞之间的串扰。作为防御机制，肠道上皮细胞产生粘膜屏障，使微生物群与宿主免疫细胞分离并降低肠道通透性。肠道菌群与粘膜免疫系统之间相互作用的减弱会导致潜在致病的革兰氏阴性细菌及其相关代谢变化的增加，从而破坏上皮屏障并增加对感染的敏感性。肠病 肠道微生物组成的负面变化或负面变化，也会使免疫反应失调，引起炎症，氧化应激和胰岛素抵抗。随着时间的流逝，慢性营养不良和细菌及其代谢产物跨粘膜屏障的转移可能会增加2型糖尿病，心血管疾病，炎性肠病，自身免疫性疾病和各种癌症的患病率。在本文中，我们强调了肠道菌群及其代谢产物（短链脂肪酸（SCFA））在粘膜免疫中的关键作用。心血管疾病，炎症性肠病，自身免疫性疾病和各种癌症。在本文中，我们强调了肠道菌群及其代谢产物（短链脂肪酸（SCFA））在粘膜免疫中的关键作用。心血管疾病，炎症性肠病，自身免疫性疾病和各种癌症。在本文中，我们强调了肠道菌群及其代谢产物（短链脂肪酸（SCFA））在粘膜免疫中的关键作用。