Evidence map›Paper›PMID 35428807›Full record

ArticleScientific reports2022

An activation specific anti-Mac-1 designed ankyrin repeat protein improves survival in a mouse model of acute lung injury.

Patrick M Siegel, Anne-Sophie Przewosnik, Jan Wrobel, Timo Heidt, Martin Moser, Karlheinz Peter, Christoph Bode, Philipp Diehl, István Bojti

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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  3. 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

9 authors at 3 institutions in 2 countries.

Patrick M Siegel *Department of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Anne-Sophie PrzewosnikDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Jan WrobelDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Timo HeidtDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Martin MoserDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Karlheinz PeterAtherothrombosis and Vascular Biology Laboratory, Baker Heart and Diabetes Institute, Melbourne, Australia.
Christoph BodeDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
Philipp DiehlDepartment of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany.
István Bojti *Department of Cardiology and Angiology I, University Heart Center Freiburg - Bad Krozingen, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106, Freiburg, Germany. istvan.bojti@uniklinik-freiburg.de.
Universitäts-Herzzentrum Freiburg-Bad Krozingen · DEUniversity of Freiburg · DEMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acute respiratory distress syndrome (ARDS) is a life-threatening clinical condition. The number of ARDS cases has risen dramatically recently but specific treatment options are limited. ARDS is associated with an overshooting inflammatory response and neutrophils play a central role in its pathogenesis. Neutrophils express the integrin Mac-1 on their surface which adopts a resting and activated conformation depending on leukocyte activation. The aim of this study was to investigate the anti-inflammatory effects of the unique activation-specific anti-Mac-1 DARPin 'F7' in a mouse model of ARDS. ARDS was induced by intratracheal lipopolysaccharide (LPS) instillation and the acute (day 1-4) and chronic phase (day 5-10) were studied. After expression and purification, F7, a control DARPin and PBS, were applied daily via the intraperitoneal route. Survival and weight loss were recorded. Histological analysis of lung sections, flow cytometric leukocyte analysis of blood and bronchioalveolar lavage (BALF) were performed. Moreover, protein concentration and cytokine levels were determined in the BALF. Treatment with F7 improved survival and reduced weight loss significantly compared to treatment with the control DARPin or PBS. Neutrophil count in the BALF and peripheral blood were significantly reduced in mice treated with F7. Histology revealed significantly reduced pulmonary inflammation in the F7 treated group. Treatment with DARPin F7 inhibited neutrophil accumulation, reduced signs of local and systemic inflammation and improved survival in a mouse model of ARDS. F7 may be a novel anti-inflammatory drug candidate for the treatment of severe ARDS.

Indexed as

Acute Lung InjuryRespiratory Distress SyndromeAnimalsAnkyrin RepeatAnti-Inflammatory AgentsBronchoalveolar Lavage FluidDisease Models, AnimalLipopolysaccharidesLungMacrophage-1 AntigenMiceWeight LossAnti-Inflammatory AgentsLipopolysaccharidesMacrophage-1 Antigen

Identifiers

PMID35428807
PMCPMC9012056
OpenAlexW4223921613

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.