Evidence map›Paper›PMID 36275710›Full record

ArticleFrontiers in immunology2022

"Rogue" neutrophil-subset [DEspR+CD11b+/CD66b+] immunotype is an actionable therapeutic target for neutrophilic inflammation-mediated tissue injury -

Saskia Carstensen, Meike Müller, Glaiza L A Tan, Khristine Amber Pasion, Jens M Hohlfeld, Victoria L M Herrera, Nelson Ruiz-Opazo

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Observational
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  4. 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

7 authors at 2 institutions in 2 countries.

Saskia CarstensenFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Department of Biomarker Analysis and Development, Hannover, Germany.
Meike MüllerFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Department of Biomarker Analysis and Development, Hannover, Germany.
Glaiza L A TanWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston MA, United States.
Khristine Amber PasionWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston MA, United States.
Jens M HohlfeldFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Department of Biomarker Analysis and Development, Hannover, Germany.
Victoria L M HerreraWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston MA, United States.
Nelson Ruiz-OpazoWhitaker Cardiovascular Institute and Department of Medicine, Boston University School of Medicine, Boston MA, United States.
Boston University · USFraunhofer Institute for Toxicology and Experimental Medicine · DE

Funding

Boston Biomedical Innovation CenterU54HL119145 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GOLAN, DAVID E., LOSCALZO, JOSEPH · 2013 to 2021
$18.8M
NHLBI NIH HHS U54 HL119145
6 · The paper itself

Abstract

Background and objective: The correlation (Rs > 0.7) of neutrophils expressing the dual endothelin1/signal peptide receptor (DEspR+CD11b+/CD66b+) with severity of hypoxemia (SF-ratio) and multi-organ failure (SOFA-score) in patients with acute respiratory distress syndrome (ARDS) suggest the hypothesis that the DEspR+ neutrophil-subset is an actionable therapeutic target in ARDS. To test this hypothesis, we conducted Methods: We performed tests in lipopolysaccharide (LPS)-induced acute neutrophilic inflammation in three species - human, rhesus macaque, rat - with increasing dose-dependent severity. We measured DEspR+CD66b+ neutrophils in bronchoalveolar lavage fluid (BALF) in healthy volunteers (HVs) 24-hours after segmental LPS-challenge by ChipCytometry, and DEspR+CD11b+ neutrophils in whole blood and BALF in an LPS-induced transient acute lung injury (ALI) model in macaques. We determined anti-DEspR antibody efficacy Results: ChipCytometry detected increased BALF total neutrophil and DEspR+CD66b+ neutrophil counts after segmental LPS-challenge compared to baseline ( Conclusion: Detection of increased DEspR+ neutrophil-subset in human BALF after segmental LPS-challenge supports the correlation of circulating DEspR+ neutrophil counts with severity measure (SOFA-score) in ARDS. Efficacy and safety of targeted inhibition of DEspR+CD11b+ neutrophil-subset in LPS-induced transient-ALI and high-mortality encephalopathy models identify a potential therapeutic target for neutrophil-mediated secondary tissue injury.

Indexed as

Acute Lung InjuryBrain DiseasesRespiratory Distress SyndromeAnimalsHumansHypoxiaInflammationLipopolysaccharidesMacaca mulattaNeutrophilsRatsLipopolysaccharidesacute lung injuryDEspRLPS-acute inflammation tissue injury modelsLPS-brain encephalopathyneutrophil subsetsegmental LPS challenge

Identifiers

PMID36275710
PMCPMC9581391
OpenAlexW4301585217

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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.