Evidence map›Paper›PMID 36832296›Full record

ReviewDiagnostics (Basel, Switzerland)2023

Airway Epithelium: A Neglected but Crucial Cell Type in Asthma Pathobiology.

Sabita Singh, Joytri Dutta, Archita Ray, Atmaja Karmakar, Ulaganathan Mabalirajan

Open access · goldAbstract readReview
In one paragraph

Review in Diagnostics (Basel, Switzerland), 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 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Allergen-induced activation of epithelial P2YThe Journal of allergy and clinical immunology · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Body Weight and Allergic Asthma: A Narrative Review.Journal of clinical medicine · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. ATP functions as a primary alarmin in allergen-induced type 2 immunity.American journal of physiology. Cell physiology · 2023
    Review
  17. Review
  18. Article
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 1 institution in 1 country.

Sabita SinghMolecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, West Bengal, India.
Joytri DuttaMolecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, West Bengal, India.
Archita RayMolecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, West Bengal, India.
Atmaja KarmakarMolecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, West Bengal, India.
Ulaganathan MabalirajanMolecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, West Bengal, India.ORCID 0000-0002-2547-1023
Indian Institute of Chemical Biology · IN

Funding

Council of Scientific and Industrial Research MLP137Science and Engineering Research Board GAP432
6 · The paper itself

Abstract

The features of allergic asthma are believed to be mediated mostly through the Th2 immune response. In this Th2-dominant concept, the airway epithelium is presented as the helpless victim of Th2 cytokines. However, this Th2-dominant concept is inadequate to fill some of the vital knowledge gaps in asthma pathogenesis, like the poor correlation between airway inflammation and airway remodeling and severe asthma endotypes, including Th2-low asthma, therapy resistance, etc. Since the discovery of type 2 innate lymphoid cells in 2010, asthma researchers started believing in that the airway epithelium played a crucial role, as alarmins, which are the inducers of ILC2, are almost exclusively secreted by the airway epithelium. This underscores the eminence of airway epithelium in asthma pathogenesis. However, the airway epithelium has a bipartite functionality in sustaining healthy lung homeostasis and asthmatic lungs. On the one hand, the airway epithelium maintains lung homeostasis against environmental irritants/pollutants with the aid of its various armamentaria, including its chemosensory apparatus and detoxification system. Alternatively, it induces an ILC2-mediated type 2 immune response through alarmins to amplify the inflammatory response. However, the available evidence indicates that restoring epithelial health may attenuate asthmatic features. Thus, we conjecture that an epithelium-driven concept in asthma pathogenesis could fill most of the gaps in current asthma knowledge, and the incorporation of epithelial-protective agents to enhance the robustness of the epithelial barrier and the combative capacity of the airway epithelium against exogenous irritants/allergens may mitigate asthma incidence and severity, resulting in better asthma control.

Indexed as

airway epitheliumalarminsallergic asthma

Identifiers

PMID36832296
PMCPMC9955099
OpenAlexW4321459844

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.