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肠道益生菌对急性肝损伤患者肠道免疫功能的影响 被引量:1

Effect of intestinal probiotics on intestinal immune function in patients with acute liver injury
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摘要 急性肝损伤是指各种原因引起的肝脏功能的急性异常,持续的肝损伤容易引发急性肝衰竭。以往的研究已证实急性肝损伤后肠道菌群的失衡和易位与该病的发生、发展密切相关。肠道益生菌的减少及炎症状态下辅助性T细胞(helper T cell,Th)17分泌白细胞介素(interleukin,IL)-17功能活跃,参与了疾病病情的加重进程,此时补充肠道益生菌有可能通过调节色氨酸(tryptophan,Trp)-犬尿酸(kynurenine,KYN)代谢通路,进而影响表达于肠黏膜免疫细胞的芳香烃受体(aromatic hydrocarbon receptor,AHR)的激活过程。AHR作为连接肠道菌群与肠道免疫的关键点参与了肠黏膜免疫屏障功能的调节。活化的AHR通过对调节性T细胞(regulatory T cell,Treg)的诱导对Th17细胞的功能产生影响,使肠道益生菌实现对肠道免疫屏障的保护作用,现就肠道益生菌对急性肝损伤患者肠道免疫功能的潜在调节机制进行概述。 Acute liver injury refers to acute abnormal liver function caused by various reasons.Persistent liver injury can easily lead to acute liver failure.Previous studies have confirmed that the imbalance and translocation of intestinal flora after acute liver injury are closely related to the occurrence and development of the disease.The decrease of intestinal probiotics and the active secretion of interleukin(IL)-17 by helper T cell(Th)17 in inflammatory state are involved in the further aggravation of the disease.At the same time,supplementation of intestinal probiotics may affect the activation of aromatic hydrocarbon receptor(AHR)expressed in intestinal mucosal immune cells by regulating tryptophan(TRP)-kynurenine(KYN)metabolic pathway.AHR participates in the regulation of intestinal mucosal immune barrier function.Activated AHR affects the function of Th17 cells by inducing regulatory T cells(Treg),so that intestinal probiotics can protect intestinal immune barrier.This review summarized the potential regulatory mechanism of intestinal probiotics on intestinal immune function in patients with acute liver injury was described.
作者 周志儒 王琦 Zhou Zhiru;Wang Qi(The Graduate School,Shanxi Medical University,Taiyuan 030000,China;Digestive Department,the second Hospital of Shanxi Medical University,Taiyuan 030000,China)
出处 《国际免疫学杂志》 CAS 2020年第5期575-580,共6页 International Journal of Immunology
关键词 肠道益生菌 犬尿酸 芳香烃受体 辅助性T细胞 调节性T细胞 急性肝损伤 Intestinal probiotics Kynurenine Aromatic hydrocarbon receptor Helper T cells Regulatory T cells Acute liver injury
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