Evidence map›Paper›PMID 35379853›Full record

ArticleScientific reports2022

A targetable 'rogue' neutrophil-subset, [CD11b+DEspR+] immunotype, is associated with severity and mortality in acute respiratory distress syndrome (ARDS) and COVID-19-ARDS.

Victoria L M Herrera, Allan J Walkey, Mai Q Nguyen, Christopher M Gromisch, Julie Z Mosaddhegi, Matthew S Gromisch, Bakr Jundi, Soeren Lukassen, Saskia Carstensen, Ridiane Denis and 11 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 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
0.9field-weighted citation impact, top 28% 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, 11 citations in OpenAlex.

  1. Observational
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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

21 authors at 7 institutions in 2 countries.

Victoria L M HerreraWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA. vherrera@bu.edu.
Allan J WalkeySection of Pulmonary and Critical Care, Department of Medicine, Boston University School of Medicine, and Boston Medical Center, Boston, MA, USA.
Mai Q NguyenWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Christopher M GromischWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Julie Z MosaddhegiWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Matthew S GromischWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA.
Bakr JundiPulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Soeren LukassenCenter for Digital Health, Berlin Institute of Health and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany.
Saskia CarstensenFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
Ridiane DenisGeneral Clinical Research Center, Boston University School of Medicine, Boston, MA, USA.
Anna C BelkinaDepartment of Pathology and Laboratory Medicine, Flow Cytometry Core Facility, Boston University School of Medicine, Boston, MA, USA.
Rebecca M BaronPulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Mayra Pinilla-VeraPulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Meike MuellerFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany.
W Taylor KimberlyDivision of Neurocritical Care, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Joshua N GoldsteinDepartment of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Irina LehmannMolecular Epidemiology Unit, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin and Berlin Institute of Health (BIH), Berlin, Germany.
Angela R ShihDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Roland EilsCenter for Digital Health, Berlin Institute of Health and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Zu Berlin, Berlin, Germany.
Bruce D LevyPulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Nelson Ruiz-OpazoWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston, MA, USA. nruizo@bu.edu.
Boston University · USHarvard University · USFraunhofer Institute for Toxicology and Experimental Medicine · DEFreie Universität Berlin · DEMassachusetts General Hospital · USBrigham and Women's Hospital · USCharité - Universitätsmedizin Berlin · DE

Funding

Project-005UL1TR001430 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BAIR-MERRITT, MEGAN H, CENTER, DAVID M. · 2015 to 2024
$52.3M
Boston Biomedical Innovation CenterU54HL119145 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GOLAN, DAVID E., LOSCALZO, JOSEPH · 2013 to 2021
$18.8M
NCATS NIH HHS UL1 TR001430NHLBI NIH HHS U54 HL119145NIH HHS NIH 1UL1TR001430
6 · The paper itself

Abstract

Neutrophil-mediated secondary tissue injury underlies acute respiratory distress syndrome (ARDS) and progression to multi-organ-failure (MOF) and death, processes linked to COVID-19-ARDS. This secondary tissue injury arises from dysregulated neutrophils and neutrophil extracellular traps (NETs) intended to kill pathogens, but instead cause cell-injury. Insufficiency of pleiotropic therapeutic approaches delineate the need for inhibitors of dysregulated neutrophil-subset(s) that induce subset-specific apoptosis critical for neutrophil function-shutdown. We hypothesized that neutrophils expressing the pro-survival dual endothelin-1/VEGF-signal peptide receptor, DEspR, are apoptosis-resistant like DEspR+ cancer-cells, hence comprise a consequential pathogenic neutrophil-subset in ARDS and COVID-19-ARDS. Here, we report the significant association of increased peripheral DEspR+CD11b+ neutrophil-counts with severity and mortality in ARDS and COVID-19-ARDS, and intravascular NET-formation, in contrast to DEspR[-] neutrophils. We detect DEspR+ neutrophils and monocytes in lung tissue patients in ARDS and COVID-19-ARDS, and increased neutrophil RNA-levels of DEspR ligands and modulators in COVID-19-ARDS scRNA-seq data-files. Unlike DEspR[-] neutrophils, DEspR+CD11b+ neutrophils exhibit delayed apoptosis, which is blocked by humanized anti-DEspR-IgG4

Indexed as

COVID-19Extracellular TrapsRespiratory Distress SyndromeHumansImmunophenotypingNeutrophils

Identifiers

PMID35379853
PMCPMC8977568
OpenAlexW4225477730

What Socratic holds

Textmetadata
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 Socratic graph.