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口咽和肠道微生物群失调对伴有先前感染的急性缺血性卒中全身炎症反应和短期预后的影响。

The impact of dysbiosis in oropharyngeal and gut microbiota on systemic inflammatory response and short-term prognosis in acute ischemic stroke with preceding infection.

作者信息

He Qiuxing, Li Guoshun, Zhao Jiasheng, Zhu Huishan, Mo Huanhao, Xiong Zhanshi, Zhao Zhan, Chen Jingyi, Ning Weimin

机构信息

Department of Neurology, Dongguan Hospital of Guangzhou University of Chinese Medicine, Dongguan, China.

South China Research Center for Acupuncture and Moxibustion, Medical College of Acu-Moxi and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Front Microbiol. 2024 Aug 22;15:1432958. doi: 10.3389/fmicb.2024.1432958. eCollection 2024.

DOI:10.3389/fmicb.2024.1432958
PMID:39238889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11374613/
Abstract

BACKGROUND

Stroke is a devastating disease and ranks as the second leading cause of death and disability globally. Several studies have shown that preceding infection (PI) of upper respiratory tract are strongly associated with acute ischemic stroke (AIS). However, the clinical implications and underlying pathological mechanisms remain unclear.

METHODS

In this study, 16S rRNA gene sequencing was employed to compare the structural characteristics of oropharyngeal and gut microbiota in AIS patients with or without PI and normal controls (NCs; 30 cases each), and systemic inflammatory markers were detected to explore the relationship between upper respiratory tract infections (URTIs) and subsequent stroke severity and functional outcome and the potential mechanism.

RESULTS

We found that patients with AIS-PI exhibited elevated serum WBC, NE, CRP, and Hcy levels, as well as a higher 90-day mRS score. Oropharyngeal and gut microbiota analysis showed that AIS and AIS-PI patients exhibited increased microbial richness in sequence. Principal coordinate analysis of the microbiota demonstrated significant differences in microbiota composition among the three groups. In AIS-PI patients, , , , , and were significantly enriched in the gut. Opportunistic pathogens, including , sp., and , were found to be significantly enriched in the oropharynx. The dysregulated microbiota were positively correlated with systemic inflammatory markers, stroke severity, and poor prognosis. In contrast, short-chain fatty acid-producing bacteria , , , , and were enriched in NCs. Their abundances were negatively correlated with systemic inflammatory markers, stroke severity and poor prognosis.

CONCLUSION

Our findings suggest that PIs of the upper respiratory tract may contribute to poor short-term functional outcome in AIS patients by causing disturbance of the oropharyngeal and gut microbiota and promoting elevated systemic inflammation levels.

摘要

背景

中风是一种极具破坏性的疾病,是全球第二大致死和致残原因。多项研究表明,上呼吸道前驱感染(PI)与急性缺血性中风(AIS)密切相关。然而,其临床意义和潜在病理机制仍不清楚。

方法

在本研究中,采用16S rRNA基因测序比较有或无PI的AIS患者与正常对照(NCs;每组30例)的口咽和肠道微生物群的结构特征,并检测全身炎症标志物,以探讨上呼吸道感染(URTIs)与随后中风严重程度和功能结局之间的关系以及潜在机制。

结果

我们发现AIS-PI患者的血清白细胞、中性粒细胞、C反应蛋白和同型半胱氨酸水平升高,以及90天改良Rankin量表(mRS)评分更高。口咽和肠道微生物群分析表明,AIS和AIS-PI患者的微生物序列丰富度增加。微生物群的主坐标分析显示三组之间微生物群组成存在显著差异。在AIS-PI患者中,[具体物种1]、[具体物种2]、[具体物种3]、[具体物种4]和[具体物种5]在肠道中显著富集。包括[具体物种6]、[具体物种7]属和[具体物种8]在内的机会性病原体在口咽中显著富集。失调的微生物群与全身炎症标志物、中风严重程度和预后不良呈正相关。相比之下,产生短链脂肪酸的细菌[具体物种9]、[具体物种10]、[具体物种11]、[具体物种12]和[具体物种13]在NCs中富集。它们的丰度与全身炎症标志物、中风严重程度和预后不良呈负相关。

结论

我们的研究结果表明,上呼吸道PI可能通过导致口咽和肠道微生物群紊乱以及促进全身炎症水平升高,导致AIS患者短期功能结局不良。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/74f50043c212/fmicb-15-1432958-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/25ff4da6e253/fmicb-15-1432958-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/2d706ebd199a/fmicb-15-1432958-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/d0b6c0e82c78/fmicb-15-1432958-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/efa0aa470378/fmicb-15-1432958-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/88e777420f2e/fmicb-15-1432958-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/74f50043c212/fmicb-15-1432958-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/25ff4da6e253/fmicb-15-1432958-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/2d706ebd199a/fmicb-15-1432958-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/d0b6c0e82c78/fmicb-15-1432958-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/efa0aa470378/fmicb-15-1432958-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/88e777420f2e/fmicb-15-1432958-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/88a6/11374613/74f50043c212/fmicb-15-1432958-g006.jpg

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