Evidence map›Paper›PMID 39337843›Full record

ArticleLife (Basel, Switzerland)2024

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

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

Abstract read
In one paragraph

Article in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Sandeep SilawalInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg and Salzburg, General Hospital Nuremberg, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.
Clemens GögeleInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg and Salzburg, General Hospital Nuremberg, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.ORCID 0000-0002-7086-9743
Petr PelikanInstitute for Pathology, Paracelsus Medical University, Nuremberg, General Hospital, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.
Christian WernerInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg and Salzburg, General Hospital Nuremberg, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.
Georgia LevidouInstitute for Pathology, Paracelsus Medical University, Nuremberg, General Hospital, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.ORCID 0000-0002-1398-178X
Raman MahatoDepartment of Emergency and Intensive Care Medicine, Klinikum Ernst von Bergmann, Charlottenstraße 72, 14467 Potsdam, Germany.
Gundula Schulze-TanzilInstitute of Anatomy and Cell Biology, Paracelsus Medical University, Nuremberg and Salzburg, General Hospital Nuremberg, Prof. Ernst Nathan Str. 1, 90419 Nuremberg, Germany.ORCID 0000-0002-9807-9532

Funding

Dr. Ernst & Anita foundation no number
6 · The paper itself

Abstract

backgroundA 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.

objectiveIn 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.

methodsHistochemical staining and immunolabeling of CD55 protein were performed.

resultsThe 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.

conclusionsEven 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.

Indexed as

ARDSCD55histologyimmunofluorescencelungsSARS-CoV-2

Identifiers

PMID39337843
PMCPMC11432792

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.