Evidence map›Paper›PMID 34710339›Full record

ArticleAmerican journal of respiratory cell and molecular biology2022

Tissue Proteomic Analysis Identifies Mechanisms and Stages of Immunopathology in Fatal COVID-19.

Clark D Russell, Asta Valanciute, Naomi N Gachanja, Jillian Stephen, Rebekah Penrice-Randal, Stuart D Armstrong, Sara Clohisey, Bo Wang, Wael Al Qsous, William A Wallace and 9 more

Open access · hybridAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  3. Basophils activate oncostatin M receptor-expressing vagal sensory neurons.The Journal of allergy and clinical immunology · 2026
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  13. BASOPHILS ACTIVATE PRURICEPTOR-LIKE VAGAL SENSORY NEURONS.bioRxiv : the preprint server for biology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 7 institutions in 2 countries.

Clark D RussellUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.ORCID 0000-0002-9873-8243
Asta ValanciuteUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.
Naomi N GachanjaUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.
Jillian StephenUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.
Rebekah Penrice-RandalInstitute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, United Kingdom.ORCID 0000-0002-0653-2097
Stuart D ArmstrongInstitute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, United Kingdom.ORCID 0000-0002-3862-1801
Sara ClohiseyRoslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, United Kingdom.ORCID 0000-0001-7489-9846
Bo WangRoslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, United Kingdom.ORCID 0000-0002-1580-797X
Wael Al QsousDepartment of Pathology, Western General Hospital, Edinburgh, United Kingdom.ORCID 0000-0002-5212-2574
William A WallaceDepartment of Pathology.
Gabriel C OniscuEdinburgh Transplant Centre.
Jo StevensRoslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, United Kingdom.
David J HarrisonSchool of Medicine, University of St. Andrews, North Haugh, St. Andrews, United Kingdom.ORCID 0000-0001-9041-9988
Kevin DhaliwalUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.ORCID 0000-0002-3925-3174
Julian A HiscoxInstitute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Liverpool, United Kingdom.ORCID 0000-0002-6582-0275
J Kenneth BaillieRoslin Institute, University of Edinburgh, Easter Bush Campus, Midlothian, United Kingdom.ORCID 0000-0001-5258-793X
Ahsan R AkramUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.ORCID 0000-0003-4605-1682
David A DorwardUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.ORCID 0000-0002-4658-8829
Christopher D LucasUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, Edinburgh BioQuarter, Edinburgh, United Kingdom.ORCID 0000-0002-7523-0295
Queen's Medical Centre · GBRoslin Institute · GBUniversity of Liverpool · GBAgency for Science, Technology and Research · SGMRC Centre for Regenerative Medicine · GBUniversity of St Andrews · GBWestern General Hospital · GB

Funding

Cancer Research UK 24867Chief Scientist Office COV/EDI/20/10Medical Research Council MC_PC_19025Medical Research Council MC_PC_19059Medical Research Council MR/V028790/1Wellcome TrustWellcome Trust 206566/Z/17/ZWellcome Trust 214178/Z/18/Z
6 · The paper itself

Abstract

Immunopathology occurs in the lung and spleen in fatal coronavirus disease (COVID-19), involving monocytes/macrophages and plasma cells. Antiinflammatory therapy reduces mortality, but additional therapeutic targets are required. We aimed to gain mechanistic insight into COVID-19 immunopathology by targeted proteomic analysis of pulmonary and splenic tissues. Lung parenchymal and splenic tissue was obtained from 13 postmortem examinations of patients with fatal COVID-19. Control tissue was obtained from cancer resection samples (lung) and deceased organ donors (spleen). Protein was extracted from tissue by phenol extraction. Olink multiplex immunoassay panels were used for protein detection and quantification. Proteins with increased abundance in the lung included MCP-3, antiviral TRIM21, and prothrombotic TYMP. OSM and EN-RAGE/S100A12 abundance was correlated and associated with inflammation severity. Unsupervised clustering identified "early viral" and "late inflammatory" clusters with distinct protein abundance profiles, and differences in illness duration before death and presence of viral RNA. In the spleen, lymphocyte chemotactic factors and CD8A were decreased in abundance, and proapoptotic factors were increased. B-cell receptor signaling pathway components and macrophage colony stimulating factor (CSF-1) were also increased. Additional evidence for a subset of host factors (including DDX58, OSM, TYMP, IL-18, MCP-3, and CSF-1) was provided by overlap between

Indexed as

AgedAged, 80 and overAutopsyCOVID-19FemaleGene Expression RegulationHumansInflammationLungMaleProteomicsSARS-CoV-2SpleenCOVID-19inflammationlungmacrophagesproteomics

Identifiers

PMID34710339
PMCPMC8845132
OpenAlexW3211183869

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.