详细信息
Targeted modulation of intestinal barrier and mucosal immune-related microbiota attenuates IgA nephropathy progression ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Targeted modulation of intestinal barrier and mucosal immune-related microbiota attenuates IgA nephropathy progression
作者:Zhang, Ran[1,2];Tang, Yuyan[3];Feng, Xiangru[1];Lu, Xiaoxuan[1];Zhao, Mengyao[1,2];Jin, Jiayang[1,4];Ji, Xiaoguo[1,2];He, Haidong[3];Zhao, Liming[1,4]
机构:[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai, Peoples R China;[2]East China Univ Sci & Technol, Shanghai Frontiers Sci Ctr Optogenet Tech Cell Met, Sch Pharm, Shanghai, Peoples R China;[3]Fudan Univ, Minhang Hosp, Dept Nephrol, Shanghai, Peoples R China;[4]Shanghai Collaborat Innovat Ctr Biomfg Technol SCI, Shanghai, Peoples R China
年份:2025
卷号:17
期号:1
外文期刊名:GUT MICROBES
收录:;WOS:【SCI-EXPANDED(收录号:WOS:001407351700001)】;
基金:We are most grateful to all the volunteers involved in the study. We would also like to acknowledge the staff of the Minhang Hospital, Fudan University, and the State Key Laboratory of Bioreactor Engineering, ECUST, for their assistance in the study.
语种:英文
外文关键词:IgA nephropathy; gut microbiota; chitooligosaccharides; kidney-gut crosstalk; human microbiota-associated mice
摘要: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 alpha-diversity and structural alterations in the gut microbiota, characterized by an increase in Shigella sonnei, Streptococcus danieliae, Desulfovibrio fairfieldensis, and a decrease in Bifidobacterium pseudolongum and Clostridium leptum. 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 (Clostridium leptum, unclassified Lachnospiraceae NK4Al36 group, unclassified Clostridia vadinBB60 group, unclassified Oscillospiraceae, and unclassified Roseburia) 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.
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