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寒冷应激通过改变肠道微生物群和代谢产物在小鼠中诱导出结肠炎样表型。

Cold stress induces colitis-like phenotypes in mice by altering gut microbiota and metabolites.

作者信息

Sun Lijuan, Wang Xueying, Zou Yuankang, He Yixuan, Liang Changting, Li Juan, Li Pu, Zhang Jianbin

机构信息

Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, School of Medicine, Northwest University, Xi'an, China.

Department of Occupational and Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, China.

出版信息

Front Microbiol. 2023 Apr 11;14:1134246. doi: 10.3389/fmicb.2023.1134246. eCollection 2023.

Abstract

INTRODUCTION

The modernized lifestyle has been paralleled by an epidemic of inflammatory bowel disease (IBD). Excessive consumption of cold beverages is especially common among the modern humans. However, whether cold stress contributes directly to the gut barrier and gut-brain axis is not clear.

METHODS

We conducted a cold stress model induced by cold water. The mice were treated with 14 consecutive days of intragastric cold or common water administration. We observed changes in gut transit and gut barrier in the colon. We also employed RNA sequencing-based transcriptomic analysis to identify the genes potentially driving gut injury, and simultaneously examined the gut microbiota and metabolites in the feces.

RESULTS

We found that cold stress disturbed the intestinal function and increased gut permeability. A set of core genes related to immune responses were consistently overexpressed in the cold stress group. Additionally, cold stress induced decreased bacterial diversity, ecological network, and increased pathogens mainly belonging to Proteobacteria. The dopamine signaling pathway-related metabolites were largely reduced in the cold stress group.

CONCLUSION

This study revealed that cold stress could trigger an IBD-like phenotype in mice, implying that cold stress is a possible risk factor for IBD development.

摘要

引言

现代生活方式伴随着炎症性肠病(IBD)的流行。过量饮用冷饮在现代人中尤为常见。然而,冷应激是否直接影响肠道屏障和肠脑轴尚不清楚。

方法

我们通过冷水诱导建立了冷应激模型。对小鼠连续14天进行胃内给予冷水或常温水处理。我们观察了结肠中肠道转运和肠道屏障的变化。我们还采用基于RNA测序的转录组分析来鉴定可能导致肠道损伤的基因,并同时检测粪便中的肠道微生物群和代谢产物。

结果

我们发现冷应激扰乱了肠道功能并增加了肠道通透性。与免疫反应相关的一组核心基因在冷应激组中持续过度表达。此外,冷应激导致细菌多样性、生态网络减少,主要属于变形菌门的病原体增加。冷应激组中多巴胺信号通路相关代谢产物大幅减少。

结论

本研究表明冷应激可在小鼠中引发类似IBD的表型,这意味着冷应激可能是IBD发生发展的一个风险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/368e/10126409/aae2420b8d78/fmicb-14-1134246-g001.jpg

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