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长期后COVID综合征的持续性肠免疫轴失调:从前性,观察性,横截面病例控制研究的见解

Max Augustin¹, Lea Picard², Dominic Rauschning³

¹Department I of Internal Medicine, Medical Faculty and University Hospital Cologne, University of Cologne 50937 Cologne, Germany; Department IV of Internal Medicine, Klinik Favoriten, 1100 Vienna Healthcare Group, Vienna, Austria; Center for Molecular Medicine Cologne (CMMC), University of Cologne 50937 Cologne, Germany; Research Lab, Faculty of Medicine, Sigmund Freud University, 1020 Vienna, Austria; German Center for Infection Research (DZIF), Partner Site Bonn-Cologne, Cologne, Germany.

Mucosal immunology

|March 7, 2026

概括

后COVID综合征 (PCS) 可能源于肠道中持续存在的SARS-CoV-2核囊蛋白,破坏免疫恒常性. 这种肠道免疫联系表明了长期COVID的新治疗点.

科学领域:

免疫学免疫学免疫学
胃肠病学胃肠病学
病毒学病毒学

背景情况:

后COVID综合征 (PCS) 的发病因子尚不清楚,怀疑病毒的持续性和免疫失调.
肠免疫轴在PCS发展中的作用需要进一步研究.

研究的目的:

调查SARS-CoV-2核蛋白在肠关联淋巴组织 (GALT) 和PCS之间存在的联系.
分析患有PCS和没有PCS的个体的终端大肠 (TI) 中免疫细胞的变化.

主要方法:

从43名SARS-CoV-2康复个体 (PCS+和PCS-),分析了周围血液 (PB) 和TI活检.
流细胞计和单核细胞的组织学检查,以评估免疫细胞群和病毒蛋白质表达.
测量佐努林和MMP-9水平,以评估肠道屏障功能和炎症.

主要成果:

在PCS+个体的TI中发现了SARS-CoV-2核体蛋白质表达的升高.
PCS+个体表现出杆细胞活性增加,阳原素水平升高,以及肠道屏障功能受损.
在TI中,不同的免疫特征包括扩张的血细胞状树突细胞,改变的NK细胞和增加的中央记忆T细胞.

结论:

在GALT中的持久的SARS-CoV-2核体蛋白可能通过破坏肠道免疫恒温来驱动PCS.
肠-免疫接口是PCS病变发生的潜在因素.
针对病毒持续性和肠道免疫平衡的治疗策略需要考虑.

关键词:

巨细胞激活激活过程血细胞状树突细胞.在COVID后出现的综合征.病毒的储存库是病毒.佐努林 (Zonulin) 是一种区域性蛋白质.

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