Evidence map›Paper›PMID 35734174›Full record

ArticleFrontiers in immunology2022

Lung Epithelial CYP1 Activity Regulates Aryl Hydrocarbon Receptor Dependent Allergic Airway Inflammation.

Francesca Alessandrini, Renske de Jong, Maria Wimmer, Ann-Marie Maier, Isis Fernandez, Miriam Hils, Jeroen T Buters, Tilo Biedermann, Ulrich M Zissler, Christian Hoffmann and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Role of Aryl Hydrocarbon Receptor in Bone Biology.International journal of tryptophan research : IJTR · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

13 authors at 3 institutions in 2 countries.

Francesca AlessandriniCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Renske de JongCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Maria WimmerCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Ann-Marie MaierCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Isis FernandezMember of the German Center of Lung Research (DZL), Partner Site, Munich, Germany.
Miriam HilsDepartment of Dermatology and Allergology Biederstein, School of Medicine, Technical University of Munich, Munich, Germany.
Jeroen T ButersCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Tilo BiedermannDepartment of Dermatology and Allergology Biederstein, School of Medicine, Technical University of Munich, Munich, Germany.
Ulrich M ZisslerCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Christian HoffmannCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Julia Esser-von-BierenCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Carsten B Schmidt-WeberCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Caspar OhnmachtCenter of Allergy and Environment (ZAUM), Technical University and Helmholtz Center Munich, Munich, Germany.
Helmholtz Zentrum München · DEGerman Center for Lung Research · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lung epithelial barrier serves as a guardian towards environmental insults and responds to allergen encounter with a cascade of immune reactions that can possibly lead to inflammation. Whether the environmental sensor aryl hydrocarbon receptor (AhR) together with its downstream targets cytochrome P450 (CYP1) family members contribute to the regulation of allergic airway inflammation remains unexplored. By employing knockout mice for AhR and for single CYP1 family members, we found that AhR

Indexed as

Cytochrome P-450 CYP1A1LungReceptors, Aryl HydrocarbonAllergensAnimalsCytochrome P-450 Enzyme SystemHumansInflammationMiceMice, KnockoutAllergensCytochrome P-450 CYP1A1Cytochrome P-450 Enzyme SystemReceptors, Aryl Hydrocarbonairway epithelial cellsaryl hydrocarbon receptorCYP1B1cytochrome P450 enzymeeosinophilialung allergy

Identifiers

PMID35734174
PMCPMC9207268
OpenAlexW4281711726

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.