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严重急性呼吸综合征冠状病毒2感染肺组织中补体调节蛋白CD55的组织学分析与检测

A Histological Analysis and Detection of Complement Regulatory Protein CD55 in SARS-CoV-2 Infected Lungs.

作者信息

Silawal Sandeep, Gögele Clemens, Pelikan Petr, Werner Christian, Levidou Georgia, Mahato Raman, Schulze-Tanzil Gundula

机构信息

Institute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg and Salzburg, General Hospital Nuremberg, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.

Institute for Pathology, Paracelsus Medical University, Nuremberg, General Hospital, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.

出版信息

Life (Basel). 2024 Aug 23;14(9):1058. doi: 10.3390/life14091058.

DOI:10.3390/life14091058
PMID:39337843
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11432792/
Abstract

BACKGROUND

A complement imbalance in lung alveolar tissue can play a deteriorating role in COVID-19, leading to acute respiratory distress syndrome (ARDS). CD55 is a transmembrane glycoprotein that inhibits the activation of the complement system at the intermediate cascade level, blocking the activity of the C3 convertase.

OBJECTIVE

In our study, lung specimens from COVID-19 and ARDS-positive COVID+/ARDS+ patients were compared with COVID-19 and ARDS-negative COVID-/ARDS- as well as COVID-/ARDS+ patients.

METHODS

Histochemical staining and immunolabeling of CD55 protein were performed.

RESULTS

The COVID-/ARDS- specimen showed higher expression and homogeneous distribution of glycosaminoglycans as well as compactly arranged elastic and collagen fibers of the alveolar walls in comparison to ARDS-affected lungs. In addition, COVID-/ARDS- lung tissues revealed stronger and homogenously distributed CD55 expression on the alveolar walls in comparison to the disrupted COVID-/ARDS+ lung tissues.

CONCLUSIONS

Even though the collapse of the alveolar linings and the accumulation of cellular components in the alveolar spaces were characteristic of COVID+/ARDS+ lung tissues, evaluating CD55 expression could be relevant to understand its relation to the disease. Furthermore, targeting CD55 upregulation as a potential therapy could be an option for post-infectious complications of COVID-19 and other inflammatory lung diseases in the future.

摘要

背景

肺泡组织中的补体失衡在新型冠状病毒肺炎（COVID-19）中可能起恶化作用，导致急性呼吸窘迫综合征（ARDS）。CD55是一种跨膜糖蛋白，可在补体系统中间级联水平抑制其激活，阻断C3转化酶的活性。

目的

在我们的研究中，将COVID-19和ARDS呈阳性的COVID+/ARDS+患者的肺标本与COVID-19和ARDS呈阴性的COVID-/ARDS-患者以及COVID-/ARDS+患者进行比较。

方法

进行CD55蛋白的组织化学染色和免疫标记。

结果

与受ARDS影响的肺相比，COVID-/ARDS-标本显示出更高的糖胺聚糖表达和均匀分布，以及肺泡壁弹性纤维和胶原纤维排列紧密。此外，与结构破坏的COVID-/ARDS+肺组织相比，COVID-/ARDS-肺组织在肺泡壁上显示出更强且均匀分布的CD55表达。

结论

尽管肺泡内衬的塌陷和肺泡腔内细胞成分的积聚是COVID+/ARDS+肺组织的特征，但评估CD55表达可能有助于理解其与疾病的关系。此外，将上调CD55作为一种潜在治疗方法，可能是未来治疗COVID-19和其他炎症性肺病感染后并发症的一种选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/83a3d044828c/life-14-01058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/7bc6a56f3f85/life-14-01058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/f169adb3d094/life-14-01058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/83a3d044828c/life-14-01058-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/7bc6a56f3f85/life-14-01058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/f169adb3d094/life-14-01058-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7753/11432792/83a3d044828c/life-14-01058-g003.jpg

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Complement and complement regulatory proteins are upregulated in lungs of COVID-19 patients.补体和补体调节蛋白在 COVID-19 患者的肺部中上调。
Pathol Res Pract. 2023 Jul;247:154519. doi: 10.1016/j.prp.2023.154519. Epub 2023 May 8.
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Molecular basis of differential receptor usage for naturally occurring CD55-binding and -nonbinding coxsackievirus B3 strains.差异受体利用的分子基础：天然结合和不结合 CD55 的柯萨奇病毒 B3 株。
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