Evidence map›Paper›PMID 36084115›Full record

ArticlePloS one2022

Correlation of alpha-1 antitrypsin levels and exosome associated neutrophil elastase endothelial injury in subjects with SARS-CoV2 infection.

Jorge Lascano, Regina Oshins, Christina Eagan, Zerka Wadood, Xiao Qiang, Tammy Flagg, Yogesh Scindia, Borna Mehrad, Mark Brantly, Nazli Khodayari

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 17% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Observational
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  8. Extracellular Vesicles and Their Role in Lung Infections.International journal of molecular sciences · 2023
    Review
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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

10 authors at 1 institution in 1 country.

Jorge LascanoDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Regina OshinsDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Christina EaganDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Zerka WadoodDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Xiao QiangMilliporeSigma, R and D Department, Burlington, MO, United States of America.
Tammy FlaggDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Yogesh ScindiaDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Borna MehradDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.ORCID 0000-0001-5198-065X
Mark BrantlyDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.
Nazli KhodayariDivision of Pulmonary, Critical Care, and Sleep Medicine, University of Florida, Gainesville, United States of America.ORCID 0000-0002-4659-1622
University of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevere acute respiratory syndrome caused by a novel coronavirus 2 (SARS-CoV-2) has infected more than 18 million people worldwide. The activation of endothelial cells is a hallmark of signs of SARS-CoV-2 infection that includes altered integrity of vessel barrier and endothelial inflammation.

objectivesPulmonary endothelial activation is suggested to be related to the profound neutrophil elastase (NE) activity, which is necessary for sterilization of phagocytosed bacterial pathogens. However, unopposed activity of NE increases alveolocapillary permeability and extracellular matrix degradation. The uncontrolled protease activity of NE during the inflammatory phase of lung diseases might be due to the resistance of exosome associated NE to inhibition by alpha-1 antitrypsin.

method31 subjects with a diagnosis of SARS-CoV2 infection were recruited in the disease group and samples from 30 voluntaries matched for age and sex were also collected for control.

resultsWe measured the plasma levels of exosome-associated NE in SARS-CoV-2 patients which, were positively correlated with sign of endothelial damage in those patients as determined by plasma levels of LDH. Notably, we also found strong correlation with plasma levels of alpha-1 antitrypsin and exosome-associated NE in SARS-CoV-2 patients. Using macrovascular endothelial cells, we also observed that purified NE activity is inhibited by purified alpha-1 antitrypsin while, NE associated with exosomes are resistant to inhibition and show less sensitivity to alpha-1 antitrypsin inhibitory activity, in vitro.

conclusionsOur results point out the role of exosome-associated NE in exacerbation of endothelial injury in SARS-CoV-2 infection. We have demonstrated that exosome-associated NE could be served as a new potential therapeutic target of severe systemic manifestations of SARS-CoV-2 infection.

Indexed as

alpha 1-Antitrypsin DeficiencyCOVID-19Exosomesalpha 1-AntitrypsinEndothelial CellsHumansLeukocyte ElastaseRNA, ViralSARS-CoV-2alpha 1-AntitrypsinLeukocyte ElastaseRNA, Viral

Identifiers

PMID36084115
PMCPMC9462798
OpenAlexW4295517916

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.