Faecal hsa-miR-7704 inhibits the growth and adhesion of Bifidobacterium longum by suppressing ProB and aggravates hepatic encephalopathy
文献类型： 外文期刊
作者： Wang, Yuchong 1 ; Li, Yuyu 1 ; Lv, Longxian 1 ; Zhu, Liying 2 ; Hong, Liang 1 ; Wang, Xueyao 3 ; Zhang, Yu 1 ; Wang, Xin 2 ; Diao, Hongyan 1 ;
作者机构： 1.Zhejiang Univ, Affiliated Hosp 1, Collaborat Innovat Ctr Diag & Treatment Infect Dis, State Key Lab Diag & Treatment Infect Dis,Natl Cli, Hangzhou 310003, Peoples R China
2.Zhejiang Acad Agr Sci, Inst Food Sci, State Key Lab Managing Biot & Chem Threats Qual &, Hangzhou 310021, Peoples R China
3.Jinan Microecol Biomed Shandong Lab, Jinan, Shandong, Peoples R China
期刊名称：NPJ BIOFILMS AND MICROBIOMES （ 影响因子：9.2； 五年影响因子：9.4 ）
ISSN：
年卷期： 2024 年 10 卷 1 期
页码：
收录情况： SCI
摘要： Both gut microbiome and microRNAs (miRNAs) play a role in the development of hepatic encephalopathy (HE). However, the functional link between the microbiome and host-derived miRNAs in faeces remains poorly understood. In the present study, patients with HE had an altered gut microbiome and faecal miRNAs compared with patients with chronic hepatitis B. Transferring faeces and faecal miRNAs from patients with HE to the recipient mice aggravated thioacetamide-induced HE. Oral gavage of hsa-miR-7704, a host-derived miRNA highly enriched in faeces from patients with HE, aggravated HE in mice in a microbiome-dependent manner. Mechanistically, hsa-miR-7704 inhibited the growth and adhesion of Bifidobacterium longum by suppressing proB. B. longum and its metabolite acetate alleviated HE by inhibiting microglial activation and ammonia production. Our findings reveal the role of miRNA-microbiome axis in HE and suggest that faecal hsa-miR-7704 are potential regulators of HE progression.
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