IgA肾病与肠道微生态及肠黏膜免疫关系的研究进展  

Advances in the relationship of IgA nephropathy with intestinal microecology and intestinal mucosal immunity

作　　者：支文强 李亚峰[1] ZHI Wenqiang;LI Yafeng(The Fifth Clinical Medical School,Shanxi Medical University,Taiyuan 030012,Shanxi,China)

机构地区：[1]山西医科大学第五临床医学院,山西太原030012

出　　处：《微生物学通报》2024年第7期2271-2279,共9页Microbiology China

基　　金：国家自然科学基金(82170716)。

摘　　要：IgA肾病(Immunoglobulin A nephropathy,IgAN)是一种多种机制共同参与免疫介导的肾小球疾病,是世界上最常见的原发性肾小球疾病。此外,许多疾病与IgAN的发生和进展相关(如炎症性肠病、肝炎及HIV病毒感染、干燥综合征等),被称为继发性IgAN。目前IgAN被广泛接受的发病机制是“多重打击学说”,该学说中IgAN发病的“扳机点”即为黏膜微生态失调导致的屏障功能破坏及免疫异常。肠道黏膜作为人体黏膜系统的重要组成部分,越来越多的研究表明肠道微生态失调、黏膜屏障功能受损及免疫调节异常在IgAN的发生发展中有重要作用,与此相关的治疗靶点也是目前的研究热点。本文就目前肠道微生态与肠黏膜免疫在IgAN发病机制中作用的研究进展进行综述,以期为未来从肠道微生态及免疫功能角度寻找IgAN新的治疗靶点提供思路。Immunoglobulin A nephropathy(IgAN)is a common primary glomerular disease characterized by multifaceted,immune-mediated mechanisms.Additionally,several comorbidities,including inflammatory bowel disease,hepatitis,HIV infection,and Sjögren’s syndrome,are intricately linked to the genesis and progression of IgAN and collectively denoted as secondary IgAN.The multiple-hit hypothesis is currently the widely embraced pathogenesis framework for IgAN,positing mucosal dysbiosis-induced disruption of the barrier function and immune aberrations as pivotal triggers for IgAN pathogenesis.The intestinal mucosa,constituting a pivotal element of the mucosal system,is increasingly acknowledged for its substantive involvement in IgAN development.Perturbations in intestinal microbiota,compromised mucosal barrier integrity,and immune dysregulation are recognized as pivotal players in IgAN pathophysiology.Investigating the therapeutic targets associated with these facets currently represents a focal point in research.We comprehensively review the research advances in the roles of intestinal microecology and mucosal immunity in the pathogenesis of IgAN.This review aims to lay a foundation for exploring the novel therapeutic targets for IgAN from intestinal microbiota and immune functionality.

关 键 词：IGA肾病 肠道微生态 肠道菌群 肠黏膜免疫 代谢组学 发病机制 

分 类 号：R692.31[医药卫生—泌尿科学]