Bacteroides intestinalis mediates the sensitivity to irinotecan toxicity via tryptophan catabolites

伊立替康 毒性 拟杆菌 微生物群 代谢物 微生物学 药理学 肠道菌群 医学 生物 生物化学 内科学 免疫学 生物信息学 结直肠癌 癌症 细菌 遗传学
作者
Yuanlong Hou,Hao Wu,Zhuangyi Zhang,Jie Wang,Qifan Chen,Chun‐Ang Lian,Dandan He,Ziguang Li,Wei Wei,Xin Lin,Daming Sun,Baoshan Cao,Ting Xu,Min Cai,Guangji Wang,Xueli Zhang,Liping Duan,Haiping Hao,Xiao Zheng
出处
期刊:Gut [BMJ]
卷期号:: gutjnl-2024 被引量:1
标识
DOI:10.1136/gutjnl-2024-334699
摘要

Background Late-onset diarrhoea remains a poorly managed concern for clinical irinotecan therapy. Although bacterial β-glucuronidases (β-GUS) mediated SN-38 production is prevailingly thought to mediate intestinal toxicity, β-GUS inhibitors confer limited benefits in the clinic. Objective This study aimed to explore the role and mechanism of endogenous bacterial metabolites in susceptibility to irinotecan toxicity. Design Gut microbiota profiles and metabolites in patients with colorectal cancer (CRC) with or without diarrhoea were investigated via 16S rRNA sequencing, shotgun metagenomics and metabolomics. The role of microbial metabolites was investigated in mice by metabolic bioengineering and intestinal organoid culture. The mechanism of microbial metabolites on intestinal stem cells was investigated by transcriptional profiling and chemical intervention. Results Gut microbial configuration was differentially remodelled in diarrhoea and non-diarrhoea patients with irinotecan therapy, and the susceptibility was transmissible to recipient mice via transplantation of baseline faecal microbiome. Bacteroides intestinalis ( B. intestinalis ) was notably expanded in the diarrhoea-prone cohorts as well as in irinotecan-treated mice. B. intestinalis colonisation sensitised intestinal epithelia to irinotecan-induced chemical injury, partially via tryptophan metabolite indole-3-acetate (IAA). Both B. intestinalis and bioengineered bacteria that produce IAA exacerbated irinotecan-induced intestinal epithelial injury in mice. Mechanistically, IAA suppressed PI3K-Akt signalling, thereby impairing the renewal of intestinal epithelia under the insult of irinotecan. In clinical patients receiving irinotecan therapy, faecal IAA level was closely associated with the diarrhoea severity. Conclusion Our study uncovers the mechanism of endogenous bacterial metabolite in shaping the individual susceptibility to irinotecan toxicity and suggests IAA as a potential predictive biomarker.
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
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

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
1秒前
追光发布了新的文献求助10
1秒前
su发布了新的文献求助10
2秒前
量子星尘发布了新的文献求助10
2秒前
兴阳完成签到,获得积分10
3秒前
Luffy发布了新的文献求助10
4秒前
853210544cyz发布了新的文献求助10
4秒前
科研通AI6应助h3m采纳,获得10
5秒前
5秒前
5秒前
5秒前
单纯平露发布了新的文献求助10
6秒前
宋紫馨发布了新的文献求助10
6秒前
6秒前
6秒前
6秒前
6秒前
崔多兰发布了新的文献求助10
7秒前
7秒前
9秒前
栗子发布了新的文献求助10
9秒前
Lucas应助lyznbhh采纳,获得30
9秒前
东方诩发布了新的文献求助10
10秒前
NexusExplorer应助su采纳,获得10
10秒前
ss发布了新的文献求助10
10秒前
梁敏发布了新的文献求助10
12秒前
bkagyin应助顺心的皓轩采纳,获得10
12秒前
hvgjgfjhgjh发布了新的文献求助10
12秒前
付海燕完成签到 ,获得积分10
12秒前
12秒前
彳亍发布了新的文献求助10
12秒前
13秒前
星辰大海应助多看文献采纳,获得10
14秒前
14秒前
科研通AI6应助科研通管家采纳,获得10
14秒前
浮游应助科研通管家采纳,获得10
14秒前
悠悠应助科研通管家采纳,获得10
14秒前
思源应助科研通管家采纳,获得10
14秒前
慕青应助科研通管家采纳,获得10
14秒前
文艺的懿应助科研通管家采纳,获得10
14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
Introduction to Early Childhood Education 1000
2025-2031年中国兽用抗生素行业发展深度调研与未来趋势报告 1000
List of 1,091 Public Pension Profiles by Region 921
Identifying dimensions of interest to support learning in disengaged students: the MINE project 800
Synthesis and properties of compounds of the type A (III) B2 (VI) X4 (VI), A (III) B4 (V) X7 (VI), and A3 (III) B4 (V) X9 (VI) 500
Antihistamine substances. XXII; Synthetic antispasmodics. IV. Basic ethers derived from aliphatic carbinols and α-substituted benzyl alcohols 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 物理化学 基因 遗传学 催化作用 冶金 量子力学 光电子学
热门帖子
关注 科研通微信公众号,转发送积分 5430823
求助须知:如何正确求助?哪些是违规求助? 4543941
关于积分的说明 14189780
捐赠科研通 4462379
什么是DOI,文献DOI怎么找? 2446515
邀请新用户注册赠送积分活动 1437962
关于科研通互助平台的介绍 1414553