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肠道屏障和黏膜免疫相关微生物群的靶向调节可减轻IgA肾病进展。

Targeted modulation of intestinal barrier and mucosal immune-related microbiota attenuates IgA nephropathy progression.

作者信息

Zhang Ran, Tang Yuyan, Feng Xiangru, Lu Xiaoxuan, Zhao Mengyao, Jin Jiayang, Ji Xiaoguo, He Haidong, Zhao Liming

机构信息

State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.

Shanghai Frontiers Science Center of Optogenetic Techniques for Cell Metabolism, School of Pharmacy, East China University of Science and Technology, Shanghai, China.

出版信息

Gut Microbes. 2025 Dec;17(1):2458184. doi: 10.1080/19490976.2025.2458184. Epub 2025 Jan 28.

DOI:10.1080/19490976.2025.2458184
PMID:39875350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11776482/
Abstract

IgA nephropathy (IgAN) is related to the balance of gut microbiota. However, it is unclear whether changes in the gut microbiota can cause IgAN or attenuate its progression. This study employed IgAN and human microbiota-associated (HMA)-IgAN models to investigate the impact of IgAN on gut microbiota alteration and the mechanisms by which gut microbiota might trigger IgAN. Furthermore, this study examined the effects of chitooligosaccharides (COS) and COS formulation (COSF) with microbiota-targeting function on enhancing intestinal barrier and renal functions. These results revealed that IgAN led to a reduction in α-diversity and structural alterations in the gut microbiota, characterized by an increase in , , , and a decrease in and . There was also an imbalance in intestinal B-cell immunity and a decrease in the level of tight junction proteins (ZO-1 and Occludin). Intestinal barrier and mucosal immune-related microbiota (, and ) were enriched through targeted modulation with COS/COSF, enhancing intestinal ZO-1 expression and reducing APRIL/BAFF overexpression, thereby reducing renal damage in IgAN. In conclusion, this study clarified the kidney-gut crosstalk between gut microbiota and IgAN, providing scientific evidence for developing microbiota-targeted food interventions to improve IgAN outcomes.

摘要

IgA 肾病（IgAN）与肠道微生物群的平衡有关。然而，尚不清楚肠道微生物群的变化是否会导致 IgA 肾病或减缓其进展。本研究采用 IgA 肾病模型和人源化微生物群相关（HMA）-IgA 肾病模型，以研究 IgA 肾病对肠道微生物群改变的影响以及肠道微生物群可能引发 IgA 肾病的机制。此外，本研究还考察了具有微生物靶向功能的壳寡糖（COS）和壳寡糖制剂（COSF）对增强肠道屏障和肾功能的作用。这些结果显示，IgA 肾病导致肠道微生物群的α多样性降低和结构改变，其特征为 、 、 增加， 及 减少。肠道 B 细胞免疫也存在失衡，紧密连接蛋白（ZO-1 和闭合蛋白）水平降低。通过 COS/COSF 的靶向调节可富集肠道屏障和黏膜免疫相关的微生物群（ 、 和 ），增强肠道 ZO-1 表达并降低 APRIL/BAFF 的过表达，从而减轻 IgA 肾病中的肾损伤。总之，本研究阐明了肠道微生物群与 IgA 肾病之间的肾-肠相互作用，为开发以微生物群为靶点的食物干预措施以改善 IgA 肾病的预后提供了科学依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a8/11776482/455d57e849dd/KGMI_A_2458184_F0012_OC.jpg
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