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铊(I)暴露会扰乱C57BL/6 J小鼠的肠道微生物群、代谢谱以及局部免疫功能。

Thallium(I) exposure perturbs the gut microbiota and metabolic profile as well as the regional immune function of C57BL/6 J mice.

作者信息

Li Dong, Yao Huan, Zhu Xiaohua, Li Zeqin, Zeng Xianyin

机构信息

College of Environmental Science and Engineering, China West Normal University, Nanchong, 637009, Sichuan, China.

College of Life Science, Sichuan Agricultural University, Ya'an, Sichuan, 625014, China.

出版信息

Environ Sci Pollut Res Int. 2022 Dec;29(60):90495-90508. doi: 10.1007/s11356-022-22145-2. Epub 2022 Jul 23.

Abstract

Intestinal microbes regulate the development of diseases induced by environmental exposure. Thallium (Tl) is a highly toxic heavy metal, and its toxicity is rarely discussed in relation to gut microbes. Herein, we showed that Tl(I) exposure (10 ppm for 2 weeks) affected the alpha diversity of bacteria in the ileum, colon, and feces, but had little effect on the beta diversity of bacteria through 16S rRNA sequencing. LEfSe analysis revealed that Tl(I) exposure changed the abundance of intestinal microbiota along the digestive tract. Cecum metabolomic detection and analysis showed that Tl(I) exposure altered the abundance and composition of metabolites. In addition, the Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analysis revealed that Tl(I) exposure impaired amino acid, lipid, purine metabolism, and G protein-coupled receptor signalling pathways. A consistency test revealed a strong correlation, and a Pearson's correlation analysis showed an extensive interaction, between microorganisms and metabolites. Analysis of the intestinal immunity revealed that Tl(I) exposure suppressed the immune responses, which also had regional differences. These results identify the perturbation of the intestinal microenvironment by Tl exposure and provide a new explanation for Tl toxicity.

摘要

肠道微生物调节环境暴露诱导的疾病发展。铊(Tl)是一种剧毒重金属,其毒性很少与肠道微生物相关联进行讨论。在此,我们表明,通过16S rRNA测序,铊(I)暴露(10 ppm,持续2周)影响回肠、结肠和粪便中细菌的α多样性,但对细菌的β多样性影响较小。线性判别分析效应大小(LEfSe)分析显示,铊(I)暴露改变了沿消化道的肠道微生物群丰度。盲肠代谢组学检测与分析表明,铊(I)暴露改变了代谢物的丰度和组成。此外,京都基因与基因组百科全书(KEGG)富集分析显示,铊(I)暴露损害了氨基酸、脂质、嘌呤代谢以及G蛋白偶联受体信号通路。一致性检验显示微生物与代谢物之间存在强相关性,Pearson相关性分析显示存在广泛相互作用。肠道免疫分析表明,铊(I)暴露抑制了免疫反应,且也存在区域差异。这些结果确定了铊暴露对肠道微环境的扰动,并为铊毒性提供了新的解释。

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