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整合代谢组学与16S核糖体RNA测序以阐明强直性脊柱炎的发病机制

Integration of Metabolomics and 16S Ribosomal RNA Sequencing to Elucidate the Pathogenesis of Ankylosing Spondylitis.

作者信息

Wang Xin, Xu Haojie, Chao Yuyan, Sun Chao, Wang Tingting, Fan Xiaoyun, Tang Lin, Xu Shengqian, Xie Changhao

机构信息

Department of Rheumatology and Immunology, The First Affiliated Hospital of Bengbu Medical University, Bengbu, China.

Department of Rheumatology and Immunology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

出版信息

Immun Inflamm Dis. 2025 Mar;13(3):e70183. doi: 10.1002/iid3.70183.

Abstract

OBJECTIVE

Despite growing interest in the gut microbiota and blood metabolome in patients with ankylosing spondylitis (AS), its role remains poorly understood. Here, we investigate how microbial and metabolic alterations contribute to AS.

METHODS

Fecal microbiome data from 40 AS patients were compared with those from 40 healthy controls (HCs) using 16S ribosomal RNA (rRNA) gene sequencing. The plasma metabolic profiles were analyzed and integrated with the microbiota data to identify biological characteristics specific to AS.

RESULTS

AS patients showed significant enrichment of specific genera, including Megamonas, Elusimicrobium, Dysgonomonas, Ruminococcus_gauvreauii_group, and unclassified_Prevotellaceae. Pathways with the most differentially expressed metabolites included bile secretion; neomycin, kanamycin, and gentamicin biosynthesis; and arachidonic acid metabolism. Positive correlations between Megamonas and Elusimicrobium and metabolites such as piribedil, l-cystathionine, and crocetin dialdehyde suggested microbial enrichment in AS patients.

CONCLUSIONS

A disrupted gut microbiota and altered metabolites are present in AS patients. Integrating microbiome and metabolomic data reveals significant disruptions in AS patients, improving our understanding of its pathogenesis.

摘要

目的

尽管强直性脊柱炎(AS)患者的肠道微生物群和血液代谢组越来越受到关注,但其作用仍知之甚少。在此,我们研究微生物和代谢改变如何导致AS。

方法

使用16S核糖体RNA(rRNA)基因测序,将40例AS患者的粪便微生物组数据与40例健康对照(HCs)的数据进行比较。分析血浆代谢谱并与微生物群数据整合,以确定AS特有的生物学特征。

结果

AS患者显示特定菌属显著富集,包括巨单胞菌属、栖粪杆菌属、嗜胆菌属、戈氏瘤胃球菌群和未分类的普雷沃氏菌科。差异表达代谢物最多的通路包括胆汁分泌;新霉素、卡那霉素和庆大霉素生物合成;以及花生四烯酸代谢。巨单胞菌属与栖粪杆菌属和诸如吡贝地尔、L-胱硫醚和西红花酸二醛等代谢物之间的正相关表明AS患者中微生物富集。

结论

AS患者存在肠道微生物群紊乱和代谢物改变。整合微生物组和代谢组数据揭示了AS患者的显著紊乱,增进了我们对其发病机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e528/11947057/8fcee2d8e18d/IID3-13-e70183-g003.jpg

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