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在新冠康复后，腺苷脱氨酶通过ADA1-CD26相互作用介导内皮炎症。

Adenosine deaminase mediates endothelial inflammation via an ADA1-CD26 interaction in post-COVID.

作者信息

Kawecka Ada, Stawarska Klaudia, Romanowska-Kocejko Marzena, Żarczyńska-Buchowiecka Marta, Jędrzejewska Agata, Braczko Alicja, Deptuła Milena, Zawrzykraj Małgorzata, Król Oliwia, Frańczak Marika, Harasim Gabriela, Pikuła Michał, Hellmann Marcin, Kutryb-Zając Barbara

机构信息

Department of Biochemistry, Medical University of Gdansk, Gdańsk, Poland.

Department of Cardiac Diagnostics, Medical University of Gdansk, Gdańsk, Poland.

出版信息

Front Pharmacol. 2025 May 21;16:1578973. doi: 10.3389/fphar.2025.1578973. eCollection 2025.

DOI:10.3389/fphar.2025.1578973
PMID:40469975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12133555/
Abstract

INTRODUCTION

Adenosine deaminase (ADA) isoenzymes play a role in microvascular dysfunction following SARS-CoV-2 infection. This study analyzes the mechanisms behind ADA1-dependent endothelial inflammation in post-COVID-19 syndrome. We investigated whether immune cells from post-COVID patients could contribute to the increased total ADA activity. Additionally, we examined ADA's enzymatic and extra-enzymatic activities in human primary lung microvascular endothelial cells (HULECs) stimulated with post-COVID patients' serum.

METHODS AND RESULTS

Treatment of HULECs with sera from post-COVID patients resulted in elevated levels of the ADA1 isoenzyme and the ADA1-anchoring protein, CD26. This increase correlated with enhanced adhesion of THP-1 monocytes/macrophages to HULECs. Inhibiting the ADA1-CD26 interaction with glycoprotein-120 prevented the rise in cell-surface ADA levels in HULECs and reduced the adhesion of THP-1 cells to the endothelium. A similar effect was observed when HULECs were pre-incubated with the SARS-CoV-2 spike protein, which co-localized with CD26 in activated HULECs.

CONCLUSIONS

We propose that ADA1 promotes vascular inflammation in post-COVID-19 syndrome through both canonical and non-canonical mechanisms. On one hand, its increased enzymatic activity can suppress adenosine-dependent pathways. On the other hand, ADA1 may function as an adhesion molecule facilitating interactions between immune cells and the endothelium via ADA1-CD26 complexes.

摘要

引言

腺苷脱氨酶（ADA）同工酶在新型冠状病毒2（SARS-CoV-2）感染后的微血管功能障碍中起作用。本研究分析了新冠后综合征中ADA1依赖性内皮炎症背后的机制。我们调查了新冠后患者的免疫细胞是否会导致总ADA活性增加。此外，我们检测了用新冠后患者血清刺激的人原代肺微血管内皮细胞（HULECs）中ADA的酶活性和酶外活性。

方法与结果

用新冠后患者的血清处理HULECs导致ADA1同工酶和ADA1锚定蛋白CD26水平升高。这种增加与THP-1单核细胞/巨噬细胞与HULECs的粘附增强相关。用糖蛋白-120抑制ADA1-CD26相互作用可防止HULECs细胞表面ADA水平升高，并减少THP-1细胞与内皮的粘附。当HULECs与SARS-CoV-2刺突蛋白预孵育时观察到类似效果，该蛋白在活化的HULECs中与CD26共定位。

结论

我们提出ADA1通过经典和非经典机制促进新冠后综合征中的血管炎症。一方面，其增加的酶活性可抑制腺苷依赖性途径。另一方面，ADA1可能作为一种粘附分子，通过ADA1-CD26复合物促进免疫细胞与内皮之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/3fca143e5ae3/fphar-16-1578973-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/50a9393b068e/fphar-16-1578973-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/1e84902c0a11/fphar-16-1578973-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/3fca143e5ae3/fphar-16-1578973-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/50a9393b068e/fphar-16-1578973-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/b0a337c2d449/fphar-16-1578973-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/9f86b0ba2663/fphar-16-1578973-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/1e84902c0a11/fphar-16-1578973-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bd5/12133555/3fca143e5ae3/fphar-16-1578973-g005.jpg

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