Evidence map›Paper›PMID 34045680›Full record

ArticleMucosal immunology2021

Airway epithelial cell necroptosis contributes to asthma exacerbation in a mouse model of house dust mite-induced allergic inflammation.

Nikos Oikonomou, Martjin J Schuijs, Antonis Chatzigiagkos, Ariadne Androulidaki, Vassilis Aidinis, Hamida Hammad, Bart N Lambrecht, Manolis Pasparakis

Open access · hybridAbstract read
In one paragraph

Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Programmed Cell Death in Chronic Rhinosinusitis.Clinical and translational allergy · 2026
    Review
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  6. MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 4 countries.

Nikos OikonomouInstitute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) & Center for Molecular Medicine, University of Cologne, Cologne, Germany. noikonom@uni-koeln.de.ORCID http://orcid.org/0000-0002-4383-9741
Martjin J SchuijsLaboratory of Immunoregulation and Mucosal Immunology, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Antonis ChatzigiagkosInstitute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) & Center for Molecular Medicine, University of Cologne, Cologne, Germany.
Ariadne AndroulidakiInstitute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) & Center for Molecular Medicine, University of Cologne, Cologne, Germany.
Vassilis AidinisBiomedical Sciences Research Center 'Alexander Fleming', Vari, Greece.
Hamida HammadLaboratory of Immunoregulation and Mucosal Immunology, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Bart N LambrechtLaboratory of Immunoregulation and Mucosal Immunology, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Manolis PasparakisInstitute for Genetics, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) & Center for Molecular Medicine, University of Cologne, Cologne, Germany. pasparakis@uni-koeln.de.
University of Cologne · DEGhent University Hospital · BEAlexander Fleming Biomedical Sciences Research Center · GRVIB-UGent Center for Inflammation Research · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of epithelial cell death has emerged as a key mechanism controlling immune homeostasis in barrier surfaces. Necroptosis is a type of regulated necrotic cell death induced by receptor interacting protein kinase 3 (RIPK3) that has been shown to cause inflammatory pathologies in different tissues. The role of regulated cell death and particularly necroptosis in lung homeostasis and disease remains poorly understood. Here we show that mice with Airway Epithelial Cell (AEC)-specific deficiency of Fas-associated with death domain (FADD), an adapter essential for caspase-8 activation, developed exacerbated allergic airway inflammation in a mouse model of asthma induced by sensitization and challenge with house dust mite (HDM) extracts. Genetic inhibition of RIPK1 kinase activity by crossing to mice expressing kinase inactive RIPK1 as well as RIPK3 or MLKL deficiency prevented the development of exaggerated HDM-induced asthma pathology in FADD

Indexed as

Airway RemodelingAllergensAnimalsAsthmaBasic Helix-Loop-Helix ProteinsBiomarkersDisease Models, AnimalDisease ProgressionDisease SusceptibilityEnzyme ActivationFas-Associated Death Domain ProteinImmunoglobulin EImmunohistochemistryMiceMice, KnockoutNecroptosisAhr protein, mouseAllergensBasic Helix-Loop-Helix ProteinsBiomarkersFadd protein, mouseFas-Associated Death Domain ProteinImmunoglobulin EReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Aryl HydrocarbonRipk1 protein, mouseRipk3 protein, mouse

Identifiers

PMID34045680
PMCPMC8379077
OpenAlexW3164762147

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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.