Evidence map›Paper›PMID 32973742›Full record

ReviewFrontiers in immunology2020

Epigenetic Regulation of Airway Epithelium Immune Functions in Asthma.

Bilal Alashkar Alhamwe, Sarah Miethe, Elke Pogge von Strandmann, Daniel P Potaczek, Holger Garn

Open access · goldAbstract readReview
In one paragraph

Review 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 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
  2. Context-specific genetic effects inform endotypes and treatment in asthma.The Journal of allergy and clinical immunology · 2026
    Article
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  14. The Role of miR-144 in Inflammatory Diseases: A Review.Immunity, inflammation and disease · 2025
    Review
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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

5 authors at 4 institutions in 3 countries.

Bilal Alashkar AlhamweInstitute of Laboratory Medicine, Philipps-University Marburg, Member of the German Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center, Marburg, Germany.
Sarah MietheInstitute of Laboratory Medicine, Philipps-University Marburg, Member of the German Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center, Marburg, Germany.
Elke Pogge von StrandmannCenter for Tumor Biology and Immunology, Institute of Tumor Immunology, Philipps University Marburg, Marburg, Germany.
Daniel P PotaczekInstitute of Laboratory Medicine, Philipps-University Marburg, Member of the German Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center, Marburg, Germany.
Holger GarnInstitute of Laboratory Medicine, Philipps-University Marburg, Member of the German Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center, Marburg, Germany.
German Center for Lung Research · DEInternational University for Science and Technology · SYPhilipps University of Marburg · DEUniversities of Giessen and Marburg Lung Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a chronic inflammatory disease of the respiratory tract characterized by recurrent breathing problems resulting from airway obstruction and hyperresponsiveness. Human airway epithelium plays an important role in the initiation and control of the immune responses to different types of environmental factors contributing to asthma pathogenesis. Using pattern recognition receptors airway epithelium senses external stimuli, such as allergens, microbes, or pollutants, and subsequently secretes endogenous danger signaling molecules alarming and activating dendritic cells. Hence, airway epithelial cells not only mediate innate immune responses but also bridge them with adaptive immune responses involving T and B cells that play a crucial role in the pathogenesis of asthma. The effects of environmental factors on the development of asthma are mediated, at least in part, by epigenetic mechanisms. Those comprise classical epigenetics including DNA methylation and histone modifications affecting transcription, as well as microRNAs influencing translation. The common feature of such mechanisms is that they regulate gene expression without affecting the nucleotide sequence of the genomic DNA. Epigenetic mechanisms play a pivotal role in the regulation of different cell populations involved in asthma pathogenesis, with the remarkable example of T cells. Recently, however, there is increasing evidence that epigenetic mechanisms are also crucial for the regulation of airway epithelial cells, especially in the context of epigenetic transfer of environmental effects contributing to asthma pathogenesis. In this review, we summarize the accumulating evidence for this very important aspect of airway epithelial cell pathobiology.

Indexed as

Epigenesis, GeneticAcetylationAnimalsAsthmaBronchial HyperreactivityBronchoconstrictionDNA MethylationEpithelial CellsHistonesHumansLungMicroRNAsProtein Processing, Post-TranslationalSignal TransductionHistonesMicroRNAsairwayallergyasthmaepigeneticepitheliumhistonemethylationmicroRNA (miRNA)

Identifiers

PMID32973742
PMCPMC7461869
OpenAlexW3070704424

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.