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2型糖尿病患者肠道微生物群的特征及其与辅助性T细胞百分比的相关性。

The characteristics of intestinal microbiota in patients with type 2 diabetes and the correlation with the percentage of T-helper cells.

作者信息

Yang Fan, Li Jinyan, Wei Longqin, Qin Shenghua, Shi Qingfeng, Lu Siyan, Chu Shuyuan

机构信息

Department of Endocrinology, Guilin People's Hospital, Guilin, China.

Research Service Department, Guilin People's Hospital, Guilin, China.

出版信息

Front Microbiol. 2024 Sep 27;15:1443743. doi: 10.3389/fmicb.2024.1443743. eCollection 2024.

DOI:10.3389/fmicb.2024.1443743
PMID:39397795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11466775/
Abstract

BACKGROUND

Type 2 diabetes (T2D) is related to intestinal microflora changes and immune inflammation. We aimed to investigate the pattern of intestinal flora-systematic T helper (Th) cell linkage in T2D patients.

METHODS

Participants with T2D diagnosed by physicians and healthy controls were enrolled in the study. The Th1, Th2, and Th17 cells from the peripheral blood were assessed by flow cytometry. The feces were collected. The V3-V4 variable region of 16S rRNA was sequenced and analyzed using bioinformatics. Principal coordinate analysis (PCoA) and non-metric multidimensional scaling (NMDS) analysis were performed to assess the beta diversity. The linear discriminant analysis (LDA) effect size (LEfSe) method was applied to identify amicrobial taxon specific to T2D. The Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) was conducted to identify the metabolic pathways. A network analysis was conducted by constructing a co-occurrence network.

RESULTS

The percentages of the Th1 and Th17 cells in the peripheral blood were higher in patients with T2D than in controls. Among the top 30 genera of the intestinal microbiota, the levels of _NK4A136_group, _UCG002, and _group were lower in the patients with T2D than in controls. In the LEfSe analysis, it was observed that the and families were significantly different between patients with T2D and controls. Moreover, the Th1/Th2 ratio was positively correlated with the abundance of the and _group genera. In the network analysis, the Th1/Th2 ratio, _UCG-002, and _NK4A136_group were the important nodes.

CONCLUSION

This study provided a preliminary picture of the crosstalk between the intestinal microbiome and systematic Th cells in patients with T2D. The findings of the study suggested that the network relationship among the intestinal microbiota, metabolites, and CD4+T lymphocyte immunity was unbalanced in the patients with T2D, which might have promoted the development of T2D. This presents a therapeutic opportunity to modulate gut immune reaction and then chronic inflammation by manipulating microbiome-specific Th-cell response.

摘要

背景

2型糖尿病(T2D)与肠道微生物群变化及免疫炎症相关。我们旨在研究T2D患者肠道菌群与系统性辅助性T(Th)细胞之间的联系模式。

方法

招募经医生诊断的T2D患者和健康对照者参与研究。通过流式细胞术评估外周血中的Th1、Th2和Th17细胞。收集粪便。对16S rRNA的V3-V4可变区进行测序,并使用生物信息学进行分析。进行主坐标分析(PCoA)和非度量多维尺度分析(NMDS)以评估β多样性。应用线性判别分析(LDA)效应大小(LEfSe)方法识别T2D特有的微生物分类群。通过重建未观察状态的群落系统发育研究(PICRUSt)来识别代谢途径。通过构建共现网络进行网络分析。

结果

T2D患者外周血中Th1和Th17细胞的百分比高于对照组。在肠道微生物群的前30个属中,T2D患者中_NK4A136_group、_UCG002和_group的水平低于对照组。在LEfSe分析中,观察到T2D患者和对照组之间的 和 科存在显著差异。此外,Th1/Th2比值与 和_group属的丰度呈正相关。在网络分析中,Th1/Th2比值、_UCG-002和_NK4A136_group是重要节点。

结论

本研究初步描绘了T2D患者肠道微生物群与系统性Th细胞之间的相互作用。研究结果表明,T2D患者肠道微生物群、代谢物和CD4+T淋巴细胞免疫之间的网络关系失衡,这可能促进了T2D的发展。这为通过操纵微生物群特异性Th细胞反应来调节肠道免疫反应进而调节慢性炎症提供了治疗机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/9f3027270d5b/fmicb-15-1443743-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/d3d14dcb32d5/fmicb-15-1443743-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/38cb6542065a/fmicb-15-1443743-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/b5eeb128b728/fmicb-15-1443743-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/65e703f4e508/fmicb-15-1443743-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/ef30327d1e6a/fmicb-15-1443743-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/9f3027270d5b/fmicb-15-1443743-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/d3d14dcb32d5/fmicb-15-1443743-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/a0f8725d37a3/fmicb-15-1443743-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/38cb6542065a/fmicb-15-1443743-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/b5eeb128b728/fmicb-15-1443743-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/65e703f4e508/fmicb-15-1443743-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/ef30327d1e6a/fmicb-15-1443743-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f007/11466775/9f3027270d5b/fmicb-15-1443743-g0007.jpg

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