Evidence map›Paper›PMID 35418159›Full record

ArticleAsthma research and practice2022

A serological biomarker of type I collagen degradation is related to a more severe, high neutrophilic, obese asthma subtype.

Sarah Rank Rønnow, Jannie Marie Bülow Sand, Line Mærsk Staunstrup, Thomas Bahmer, Michael Wegmann, Lars Lunding, Janette Burgess, Klaus Rabe, Grith Lykke Sorensen, Oliver Fuchs and 7 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Asthma research and practice, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02419274 (The All Age Asthma Cohort), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% 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.

NCT02419274 recruitingnot on this map

The All Age Asthma Cohort (ALLIANCE) of the German Center for Lung Research (DZL), Adult Arm

Typeobservational_patient_registrySponsorLungenClinic GrosshansdorfRan2014 to 2030Enrolled400ConditionsAsthma
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. A macrophage-collagen fragment axis mediates subcutaneous adipose tissue remodeling in mice.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Article
  6. Highway toFrontiers in pharmacology · 2022
    Review
  7. Review
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

17 authors at 9 institutions in 4 countries.

Sarah Rank RønnowNordic Bioscience A/S, Herlev, Denmark. sar@nordicbio.com.
Jannie Marie Bülow SandNordic Bioscience A/S, Herlev, Denmark.
Line Mærsk StaunstrupNordic Bioscience A/S, Herlev, Denmark.
Thomas BahmerUniversity of Copenhagen, Health, Copenhagen, Denmark.
Michael WegmannUniversity of Copenhagen, Health, Copenhagen, Denmark.
Lars LundingUniversity of Copenhagen, Health, Copenhagen, Denmark.
Janette BurgessDivision of Asthma Mouse Model, Priority Area Asthma & Allergy, Leibniz-Center for Medicine and Biosciences Borstel, Borstel, Germany.
Klaus RabeUniversity of Copenhagen, Health, Copenhagen, Denmark.
Grith Lykke SorensenDepartment of Pathology and Medical Biology, Medical Biology Section, University Medical Center, Groningen, The Netherlands.
Oliver FuchsUniversity Childrens Hospital, Inselspital Bern, Bern, Switzerland.
Erika V MutiusDr. von Hauner Children's Hospital, University Hospital Munich, Munich, Germany.
Gesine HansenUniversity Childrens Hospital, Department of Pediatric Pneumology, Allergology and Neonatology Hannover Medical School, Hannover, Germany.
Matthias Volkmar KoppLungenClinic Grosshansdorf GmbH, Großhansdorf, Germany.
Morten KarsdalNordic Bioscience A/S, Herlev, Denmark.
Diana Julie LeemingNordic Bioscience A/S, Herlev, Denmark.
Markus WeckmannAirway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Großhansdorf, Germany.
ALLIANCE Study Group as part of the German Center of Lung Research (DZL)
Nordic Bioscience (Denmark) · DKUniversity of Copenhagen · DKLungenClinic Grosshansdorf · DEGerman Center for Lung Research · DEMedizinische Hochschule Hannover · DEMünchen Klinik · DEResearch Center Borstel - Leibniz Lung Center · DEUniversity Hospital of Bern · CHUniversity Medical Center Groningen · NL

Funding

Danish Agency for Science and Higher Education Danish Agency for Science and Higher Education
6 · The paper itself

Abstract

backgroundAsthma is a heterogeneous disease; therefore, biomarkers that can assist in the identification of subtypes and direct therapy are highly desirable. Asthma is a chronic inflammatory disease that leads to changes in the extracellular matrix (ECM) by matrix metalloproteinases (MMPs) degradation causing fragments of type I collagen that is released into circulation.

objectiveHere, we asked if MMP-generated type I collagen (C1M) was associated with subtypes of asthma.

methodsC1M was serologically assessed at baseline in the adult participants of the All Age Asthma study (ALLIANCE) (n = 233), and in The Prospective Epidemiological Risk Factor study (PERF) (n = 283). In addition, C1M was assessed in mice sensitized to ovalbumin (OVA) and challenged with OVA aerosol. C1M was evaluated in mice with and without acute neutrophilic inflammation provoked by poly(cytidylic-inosinic) acid and mice treated with CP17, a peptide inhibiting neutrophil accumulation.

resultsSerum C1M was significantly increased in asthmatics compared to healthy controls (p = 0.0005). We found the increased C1M levels in asthmatics were related to blood neutrophil and body mass index (BMI) in the ALLIANCE cohort, which was validated in the PERF cohort. When patients were stratified into obese (BMI > 30) asthmatics with high neutrophil levels and uncontrolled asthma, this group had a significant increase in C1M compared to normal-weight (BMI < 25) asthmatics with low neutrophil levels and controlled asthma (p = 0.0277). C1M was significantly elevated in OVA mice with acute neutrophilic inflammation compared to controls (P = 0.0002) and decreased in mice treated with an inhibitor of neutrophil infiltration (p = 0.047). CONCLUSION & CLINICAL RELEVANCE: C1M holds the potential to identify a subtype of asthma that relates to severity, obesity, and high neutrophils. These data suggest that C1M is linked to a subtype of overall inflammation, not only derived from the lung. The link between C1M and neutrophils were further validated in in vivo model.

trial registration(ALLIANCE, NCT02419274 ).

Identifiers

PMID35418159
PMCPMC9006548
OpenAlexW4226223927

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.