Evidence map›Paper›PMID 36354438›Full record

ArticleBiosensors2022

Genome-Wide Gene Expression Analysis Reveals Unique Genes Signatures of Epithelial Reorganization in Primary Airway Epithelium Induced by Type-I, -II and -III Interferons.

Anna Erb, Ulrich M Zissler, Madlen Oelsner, Adam M Chaker, Carsten B Schmidt-Weber, Constanze A Jakwerth

Open access · goldAbstract read
In one paragraph

Article in Biosensors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Clinical and Biological Features of a Thickened Basement Membrane Zone in Asthma.American journal of respiratory and critical care medicine · 2025
    Article
  3. The peptidoglycan ofScience translational medicine · 2025
    Article
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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

6 authors at 1 institution in 1 country.

Anna ErbCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.ORCID 0000-0002-6915-5321
Ulrich M ZisslerCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.ORCID 0000-0003-4826-3419
Madlen OelsnerCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.
Adam M ChakerCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.
Carsten B Schmidt-WeberCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.ORCID 0000-0002-3203-8084
Constanze A JakwerthCenter of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Member of the German Center for Lung Research (DZL), CPC-M, Member of the Helmholtz I&I Initiative, 85746 Munich, Germany.ORCID 0000-0002-2902-0393
Helmholtz Zentrum München · DE

Funding

Deutsche Forschungsgemeinschaft 398577603Federal Ministry of Education and Research 01KI20169A
6 · The paper itself

Abstract

Biosensors such as toll-like receptors (TLR) induce the expression of interferons (IFNs) after viral infection that are critical to the first step in cell-intrinsic host defense mechanisms. Their differential influence on epithelial integrity genes, however, remains elusive. A genome-wide gene expression biosensor chip for gene expression sensing was used to examine the effects of type-I, -II, and -III IFN stimulation on the epithelial expression profiles of primary organotypic 3D air-liquid interface airway cultures. All types of IFNs induced similar interferon-stimulated genes (ISGs): OAS1, OAS2, and IFIT2. However, they differentially induced transcription factors, epithelial modulators, and pro-inflammatory genes. Type-I IFN-induced genes were associated with cell-cell adhesion and tight junctions, while type-III IFNs promoted genes important for transepithelial transport. In contrast, type-II IFN stimulated proliferation-triggering genes associated and enhanced pro-inflammatory mediator secretion. In conclusion, with our microarray system, we provide evidence that the three IFN types exceed their antiviral ISG-response by inducing distinct remodeling processes, thereby likely strengthening the epithelial airway barrier by enhancing cross-cell-integrity (I), transepithelial transport (III) and finally reconstruction through proliferation (II).

Indexed as

Interferon Type IAntiviral AgentsEpitheliumGene ExpressionAntiviral AgentsInterferon Type Iairway epithelialepithelial integritygene expression analysis-II and -III Interferonsmicroarrayremodelingtype-I

Identifiers

PMID36354438
PMCPMC9688329
OpenAlexW4307345601

What OpenQuestion holds

Textmetadata
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.