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肠道微生物群失调与有症状患者的腰椎退行性滑脱有关。

Gut microbiome dysbiosis is associated with lumbar degenerative spondylolisthesis in symptomatic patients.

作者信息

Aboushaala Khaled, Chee Ana V, Adnan Darbaz, Toro Sheila J, Singh Harmanjeet, Savoia Andrew, Dhillon Ekamjeet S, Yuh Catherine, Dourdourekas Jake, Patel Ishani K, Vucicevic Rajko, Espinoza-Orias Alejandro A, Martin John T, Oh Chundo, Keshavarzian Ali, Albert Hanne B, Karppinen Jaro, Kocak Mehmet, Wong Arnold Y L, Goldberg Edward J, Phillips Frank M, Colman Matthew W, Williams Frances M K, Borgia Jeffrey A, Naqib Ankur, Green Stefan J, Forsyth Christopher B, An Howard S, Samartzis Dino

机构信息

Department of Orthopedic Surgery Rush University Medical Center Chicago Illinois USA.

Center for Integrated Microbiome & Chronobiology Research, Rush Medical College, Rush University Medical Center Chicago Illinois USA.

出版信息

JOR Spine. 2024 Oct 10;7(4):e70005. doi: 10.1002/jsp2.70005. eCollection 2024 Dec.

DOI:10.1002/jsp2.70005
PMID:39398942
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11467165/
Abstract

BACKGROUND

Lumbar degenerative spondylolisthesis (LDS), characterized as degeneration of the intervertebral disc and structural changes of the facet joints, is a condition with varying degrees of instability that may lead to pain, canal stenosis, and subsequent surgical intervention. However, the etiology of LDS remains inconclusive. Gut microbiome dysbiosis may stimulate systemic inflammation in various disorders. However, the role of such dysbiosis upon spine health remains under-studied. The current study assessed the association of gut microbiome dysbiosis in symptomatic patients with or without LDS.

METHODS

A cross-sectional analysis within the framework of a prospective study was performed. DNA was extracted from fecal samples collected from adult symptomatic patients with ( = 21) and without LDS ( = 12). Alpha and beta diversity assessed differences in fecal microbial community between groups. Taxon-by-taxon analysis identified microbial features with differential relative abundance between groups. Subject demographics and imaging parameters were also assessed.

RESULTS

There was no significant group differences in age, sex, race, body mass index, smoking/alcohol history, pain profiles, spinopelvic alignment, and Modic changes ( >0.05). LDS subjects had significantly higher disc degeneration severity ( = 0.018) and alpha diversity levels compared to non-LDS subjects ( = 0.002-0.003). Significant differences in gut microbial community structure were observed between groups ( = 0.046). Subjects with LDS exhibited distinct differences at the phylum level, with a significantly higher Firmicutes to Bacteroidota ratio compared to non-LDS ( = 0.003). Differential relative abundance analysis identified six taxa with significant differences between the two groups, with LDS demonstrating an increase in putative pro-inflammatory bacteria () and a decrease in anti-inflammatory bacteria (, ).

CONCLUSION

This study is the first to report a significant association of gut microbiome dysbiosis and LDS in symptomatic patients, noting pro-inflammatory bacterial taxa. This work provides a foundation for future studies addressing the role of the gut microbiome in association with spine health and disease.

摘要

背景

腰椎退行性椎体滑脱(LDS)的特征是椎间盘退变和小关节结构改变,是一种具有不同程度不稳定的病症,可能导致疼痛、椎管狭窄及后续手术干预。然而,LDS的病因仍无定论。肠道微生物群失调可能在各种疾病中引发全身炎症。然而,这种失调对脊柱健康的作用仍研究不足。本研究评估了有症状的LDS患者和无LDS患者肠道微生物群失调之间的关联。

方法

在一项前瞻性研究框架内进行横断面分析。从成年有症状的LDS患者(n = 21)和无LDS患者(n = 12)收集的粪便样本中提取DNA。α和β多样性评估了两组之间粪便微生物群落的差异。逐个分类单元分析确定了两组之间相对丰度有差异的微生物特征。还评估了受试者的人口统计学和影像学参数。

结果

在年龄、性别、种族、体重指数、吸烟/饮酒史、疼痛情况、脊柱骨盆对线和Modic改变方面,两组之间无显著差异(P>0.05)。与无LDS受试者相比,LDS受试者的椎间盘退变严重程度显著更高(P = 0.018),α多样性水平也更高(P = 0.002 - 0.003)。两组之间观察到肠道微生物群落结构存在显著差异(P = 0.046)。LDS受试者在门水平上表现出明显差异,与无LDS受试者相比,厚壁菌门与拟杆菌门的比例显著更高(P = 0.003)。差异相对丰度分析确定了两组之间有显著差异的六个分类单元,LDS组显示促炎细菌(……)增加,抗炎细菌(……)减少。

结论

本研究首次报告了有症状患者中肠道微生物群失调与LDS之间存在显著关联,并指出了促炎细菌分类单元。这项工作为未来研究肠道微生物群在脊柱健康和疾病中的作用奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/801f18549743/JSP2-7-e70005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/a58103a42ee7/JSP2-7-e70005-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/bfdfc15026e8/JSP2-7-e70005-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/801f18549743/JSP2-7-e70005-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/a58103a42ee7/JSP2-7-e70005-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/bfdfc15026e8/JSP2-7-e70005-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be1e/11467165/801f18549743/JSP2-7-e70005-g004.jpg

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