Evidence map›Paper›PMID 37759430›Full record

ReviewCells2023

The Dual Role of the Airway Epithelium in Asthma: Active Barrier and Regulator of Inflammation.

Andreas Frey, Lars P Lunding, Michael Wegmann

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.1field-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

18 citing papers in PubMed, 16 citations in OpenAlex.

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  18. Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024
    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

3 authors at 1 institution in 1 country.

Andreas FreyDivision of Mucosal Immunology and Diagnostics, Research Center Borstel, 23845 Borstel, Germany.
Lars P LundingAirway Research Center North (ARCN), German Center for Lung Research (DZL), 22927 Großhansdorf, Germany.ORCID 0000-0002-5278-3129
Michael WegmannAirway Research Center North (ARCN), German Center for Lung Research (DZL), 22927 Großhansdorf, Germany.ORCID 0000-0002-1658-1554
Research Center Borstel - Leibniz Lung Center · DE

Funding

German Center for Lung Research DZL3.0
6 · The paper itself

Abstract

Chronic airway inflammation is the cornerstone on which bronchial asthma arises, and in turn, chronic inflammation arises from a complex interplay between environmental factors such as allergens and pathogens and immune cells as well as structural cells constituting the airway mucosa. Airway epithelial cells (AECs) are at the center of these processes. On the one hand, they represent the borderline separating the body from its environment in order to keep inner homeostasis. The airway epithelium forms a multi-tiered, self-cleaning barrier that involves an unstirred, discontinuous mucous layer, the dense and rigid mesh of the glycocalyx, and the cellular layer itself, consisting of multiple, densely interconnected cell types. On the other hand, the airway epithelium represents an immunologically highly active tissue once its barrier has been penetrated: AECs play a pivotal role in releasing protective immunoglobulin A. They express a broad spectrum of pattern recognition receptors, enabling them to react to environmental stressors that overcome the mucosal barrier. By releasing alarmins-proinflammatory and regulatory cytokines-AECs play an active role in the formation, strategic orientation, and control of the subsequent defense reaction. Consequently, the airway epithelium is of vital importance to chronic inflammatory diseases, such as asthma.

Indexed as

AsthmaInflammationRespiratory MucosaAnimalsEpithelial CellsHumansasthmabarriercytokinesepitheliumIgAinflammationmucustrained immunity

Identifiers

PMID37759430
PMCPMC10526792
OpenAlexW4386443807

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.