Traumatic Brain Injury Induces Gastrointestinal Dysfunction and Dysbiosis of Gut Microbiota Accompanied by Alterations of Bile Acid Profile

失调 肠道菌群 胆汁酸 毛螺菌科 医学 炎症 内科学 微生物群 生物 厚壁菌 免疫学 生物信息学 细菌 16S核糖体RNA 遗传学
作者
Wendong You,Yuanrun Zhu,Anqi Wei,Juan Du,Yadong Wang,Peidong Zheng,Mengdi Tu,Hao Wang,Liang Wen,Xiaofeng Yang
出处
期刊:Journal of Neurotrauma [Mary Ann Liebert, Inc.]
卷期号:39 (1-2): 227-237 被引量:87
标识
DOI:10.1089/neu.2020.7526
摘要

Gastrointestinal dysfunction is a common peripheral organ complication after traumatic brain injury (TBI), yet the underlying mechanism remains unknown. TBI has been demonstrated to cause gut microbiota dysbiosis in animal models, although the impacts of gut microbiota dysbiosis on gastrointestinal dysfunction were not examined. Bile acids are key metabolites between gut microbiota and host interactions. Therefore, the aim of this study was to investigate the mechanistic links between them by detecting the alterations of gut microbiota and bile acid profile after TBI. For that, we established TBI in mice using a lateral fluid percussion injury model. Gut microbiota was examined by 16S rRNA sequencing, and bile acids were profiled by ultra-performance liquid chromatography-tandem mass spectrometry. Our results showed that TBI caused intestinal inflammation and gut barrier impairment. Alterations of gut microbiota and bile acid profile were observed. The diversity of gut microbiota experienced a time dependent change from 1 h to 7 days post-injury. Levels of bile acids in feces and plasma were decreased after TBI, and the decrease was more significant in secondary bile acids, which may contribute to intestinal inflammation. Specific bacterial taxa such as Staphylococcus and Lachnospiraceae that may contribute to the bile acid metabolic changes were identifed. In conclusion, our study suggested that TBI-induced gut microbiota dysbiosis may contribute to gastrointestinal dysfunction via altering bile acid profile. Gut microbiota may be a potential treatment target for TBI-induced gastrointestinal dysfunction.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
molihuakai的应助被真真采纳,获得10
刚刚
xiaoxiulai发布了新的文献求助10
刚刚
Maydalian完成签到,获得积分10
刚刚
wwz关闭了wwz的文献求助
刚刚
1秒前
WeirLiu发布了新的文献求助10
1秒前
踏实的又夏完成签到,获得积分10
1秒前
1111111111发布了新的文献求助10
1秒前
2秒前
酱子完成签到 ,获得积分10
2秒前
ZYX完成签到,获得积分10
2秒前
Leo_ms完成签到,获得积分10
2秒前
淡定的依丝完成签到,获得积分10
2秒前
桐桐的应助被殷勤的海采纳,获得20
2秒前
TaiZz发布了新的文献求助10
2秒前
3秒前
清风发布了新的文献求助10
3秒前
3秒前
啦啦的应助被successful采纳,获得10
3秒前
3秒前
青山完成签到 ,获得积分10
4秒前
蔚欢发布了新的文献求助10
4秒前
DW的应助被威武的人杰采纳,获得10
4秒前
麻辣啵哝完成签到,获得积分10
5秒前
5秒前
5秒前
风中的绿发布了新的文献求助10
5秒前
5秒前
吱吱完成签到,获得积分10
6秒前
FINE完成签到,获得积分10
6秒前
星晴天空完成签到,获得积分10
6秒前
zxd1999完成签到,获得积分10
6秒前
6秒前
无花果的应助被yt采纳,获得10
6秒前
梁晓宇完成签到 ,获得积分10
6秒前
Yh_alive发布了新的文献求助10
7秒前
Zpj完成签到,获得积分10
7秒前
Sc0tt发布了新的文献求助10
7秒前
7秒前
7秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Les Mantodea De Guyane 2000
Narrative Disclosure and Earnings Performance: Evidence from R&D Disclosures 1050
Preparation and Properties of Cu-Plated Graphene/Cu Composites 1000
Essays on African writing: A re-evaluation 1000
内視鏡下経鼻経蝶形骨洞手術術後SIADHに対する予防的水制限の安全性と有効性の検討 1000
Problems and Solutions for Integer and Combinatorial Optimization: Building Skills in Discrete Optimization 600
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 工程类 有机化学 化学工程 生物化学 物理 复合材料 内科学 催化作用 光电子学 人工智能 细胞生物学 无机化学 物理化学 数学
热门帖子
关注 科研通微信公众号,转发送积分 8004026
求助须知:如何正确求助?哪些是违规求助? 9455762
关于积分的说明 21157205
捐赠科研通 7576846
什么是DOI,文献DOI怎么找? 3381817
关于科研通互助平台的介绍 2514701
邀请新用户注册赠送积分活动 2416570