Evidence map›Paper›PMID 32076420›Full record

ArticleFrontiers in immunology2020

Human β-Defensin 2 Mediated Immune Modulation as Treatment for Experimental Colitis.

Louis Koeninger, Nicole S Armbruster, Karoline Sidelmann Brinch, Søren Kjaerulf, Birgitte Andersen, Carolin Langnau, Stella E Autenrieth, Dominik Schneidawind, Eduard F Stange, Nisar P Malek and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
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  19. Immunomodulatory Effects of the Tobacco Defensin NaD1.Antibiotics (Basel, Switzerland) · 2024
    Article
  20. Review

1 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 3 countries.

Louis KoeningerDepartment of Internal Medicine I, University Hospital Tübingen, Tübingen, Germany.
Nicole S ArmbrusterDepartment of Internal Medicine I, University Hospital Tübingen, Tübingen, Germany.
Karoline Sidelmann BrinchNovozymes, Bagsvaerd, Denmark.
Søren KjaerulfNovozymes, Bagsvaerd, Denmark.
Birgitte AndersenNovozymes, Bagsvaerd, Denmark.
Carolin LangnauDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Stella E AutenriethDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Dominik SchneidawindDepartment of Internal Medicine II, University Hospital Tübingen, Tübingen, Germany.
Eduard F StangeDepartment of Internal Medicine I, University Hospital Tübingen, Tübingen, Germany.
Nisar P MalekDepartment of Internal Medicine I, University Hospital Tübingen, Tübingen, Germany.
Peter NordkildDefensin Therapeutics, Copenhagen, Denmark.
Benjamin A H JensenDepartment of Medicine, Faculty of Medicine, Cardiology Axis, Quebec Heart and Lung Institute, Laval University, Quebec, QC, Canada.
Jan WehkampDepartment of Internal Medicine I, University Hospital Tübingen, Tübingen, Germany.
University Children's Hospital Tübingen · DENovozymes (Denmark) · DKUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defensins represents an integral part of the innate immune system serving to ward off potential pathogens and to protect the intestinal barrier from microbial encroachment. In addition to their antimicrobial activities, defensins in general, and human β-defensin 2 (hBD2) in particular, also exhibit immunomodulatory capabilities. In this report, we assessed the therapeutic efficacy of systemically administered recombinant hBD2 to ameliorate intestinal inflammation in three distinct animal models of inflammatory bowel disease; i.e., chemically induced mucosal injury (DSS), loss of mucosal tolerance (TNBS), and T-cell transfer into immunodeficient recipient mice. Treatment efficacy was confirmed in all tested models, where systemically administered hBD2 mitigated inflammation, improved disease activity index, and hindered colitis-induced body weight loss on par with anti-TNF-α and steroids. Treatment of lipopolysaccharide (LPS)-activated human peripheral blood mononuclear cells with rhBD2 confirmed the immunomodulatory capacity in the circulatory compartment. Subsequent analyzes revealed dendritic cells (DCs) as the main target population. Suppression of LPS-induced inflammation was dependent on chemokine receptor 2 (CCR2) expression. Mechanistically, hBD2 engaged with CCR2 on its DC target cell to decrease NF-κB, and increase CREB phosphorylation, hence curbing inflammation. To our knowledge, this is the first study showing

Indexed as

Animalsbeta-DefensinsColitisDisease Models, AnimalHumansImmunomodulationMiceRecombinant Proteinsbeta-DefensinsDEFB4A protein, humanRecombinant Proteinsantimicrobial peptideshost defense peptidesIBDinnate immunityβ-defensins

Identifiers

PMID32076420
PMCPMC7006816
OpenAlexW3003813833

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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.