Evidence map›Paper›PMID 38247549›Full record

ArticleAdvances in respiratory medicine2024

Expression of Inflammatory Genes in Murine Lungs in a Model of Experimental Pulmonary Hypertension: Effects of an Antibody-Based Targeted Delivery of Interleukin-9.

Judith Heiss, Katja Grün, Isabell Singerer, Laura Tempel, Mattia Matasci, Christian Jung, Alexander Pfeil, P Christian Schulze, Dario Neri, Marcus Franz

Open access · goldAbstract read
In one paragraph

Article in Advances in respiratory medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. 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

10 authors at 3 institutions in 2 countries.

Judith HeissDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.
Katja GrünDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.
Isabell SingererDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.
Laura TempelDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.
Mattia MatasciPhilochem AG, 8112 Otelfingen, Switzerland.
Christian JungMedical Faculty, Division of Cardiology, Pulmonology and Vascular Medicine, Heinrich-Heine University Düsseldorf, 40225 Düsseldorf, Germany.ORCID 0000-0001-8325-250X
Alexander PfeilDepartment of Internal Medicine III, University Hospital Jena, 07747 Jena, Germany.ORCID 0000-0002-2709-6685
P Christian SchulzeDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0001-9442-7141
Dario NeriPhilochem AG, 8112 Otelfingen, Switzerland.
Marcus FranzDepartment of Internal Medicine I, University Hospital Jena, Am Klinikum 1, 07747 Jena, Germany.ORCID 0000-0001-6543-4684
Jena University Hospital · DEPhilochem (Switzerland) · CHHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathogenesis of pulmonary hypertension (PH) is a multifactorial process driven by inflammation and pulmonary vascular remodeling. To target these two aspects of PH, we recently tested a novel treatment: Interleukin-9 (IL9) fused to F8, an antibody that binds to the extra-domain A of fibronectin (EDA PURPOSE: To evaluate possible F8IL9 effects on PH-associated inflammatory processes, we analysed the expression of genes involved in pulmonary immune responses.

methodsWe applied the monocrotaline (MCT) model of PH in mice (

resultsCompared with the controls, 19 genes exhibited relevant (+2.5-fold) upregulation in the PH group without treatment. Gene expression levels in F8IL9-treated lung tissue were reduced compared to the PH group without treatment. This was the case especially for CCL20, CXCL5, C-reactive protein, pentraxin related (CRP

conclusionIn accordance with the hypothesis stated above, F8IL9 treatment diminished the upregulation of some genes associated with inflammation in a PH animal model. Therefore, we hypothesize that IL9-based immunocytokine treatment will likely modulate various inflammatory pathways.

Indexed as

Hypertension, PulmonaryInterleukin-9AnimalsAntibodiesDisease Models, AnimalImmunoconjugatesInflammationLungMiceVascular RemodelingAntibodiesImmunoconjugatesInterleukin-9drug deliverygene expression analysisinflammationpulmonary hypertension

Identifiers

PMID38247549
PMCPMC10801467
OpenAlexW4390537993

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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.