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

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

Life (Basel)

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

Published: August 2024

AI Article Synopsis

  • A complement imbalance in lung alveolar tissue can worsen COVID-19, potentially leading to acute respiratory distress syndrome (ARDS), with CD55 playing a key role in regulating this process.
  • The study compared lung tissues from COVID-19 patients with and without ARDS, focusing on the expression of CD55 and the structural integrity of the alveolar walls.
  • Findings revealed that lungs from patients without ARDS had better structural organization and higher CD55 expression, suggesting that enhancing CD55 levels could be a potential therapeutic approach for COVID-19-related lung damage.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11432792PMC
http://dx.doi.org/10.3390/life14091058DOI Listing

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