Evidence map›Paper›PMID 27154200›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Effect of a chemical chaperone, tauroursodeoxycholic acid, on HDM-induced allergic airway disease.

Jalahalli M Siddesha, Emily M Nakada, Bethany R Mihavics, Sidra M Hoffman, Gurkiranjit K Rattu, Nicolas Chamberlain, Jonathon M Cahoon, Karolyn G Lahue, Nirav Daphtary, Minara Aliyeva and 4 more

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03878654 (Trial of Tauroursodeoxycholic Acid), which is not on this map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 11% 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.

NCT03878654 phase1terminatednot on this mapstarted 2019, after this paper: background citation

Trial of Tauroursodeoxycholic Acid (TUDCA) in Asthma

TypeinterventionalSponsorUniversity of VermontRan2019 to 2019Enrolled11ConditionsAsthmaArmsTauroursodeoxycholic Acid
3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. PP4 deficiency drives airway epithelial senescence via the PERK-eIF2α-ATF4-p21 axis in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Mechanisms Targeting the Unfolded Protein Response in Asthma.American journal of respiratory cell and molecular biology · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Update on the role of endoplasmic reticulum stress in asthma.American journal of translational research · 2020
    Review
  20. 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

14 authors at 2 institutions in 2 countries.

Jalahalli M SiddeshaDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Emily M NakadaDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Bethany R MihavicsDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Sidra M HoffmanDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Gurkiranjit K RattuDepartment of Biology, University of Vermont, Burlington, Vermont;
Nicolas ChamberlainDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Jonathon M CahoonDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Karolyn G LahueDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Nirav DaphtaryDepartment of Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Minara AliyevaDepartment of Medicine, University of Vermont College of Medicine, Burlington, Vermont;
David G ChapmanDepartment of Medicine, University of Vermont College of Medicine, Burlington, Vermont; Woolcock Institute of Medical Research, Sydney Medical School, University of Sydney, Sydney, Australia; and.
Dhimant H DesaiDepartment of Pharmacology, Penn State Hershey College of Medicine, Hershey, Pensylvania.
Matthew E PoynterDepartment of Medicine, University of Vermont College of Medicine, Burlington, Vermont;
Vikas AnathyDepartment of Pathology and Laboratory Medicine, University of Vermont College of Medicine, Burlington, Vermont; vikas.anathy@med.uvm.edu.
University of Vermont · USPenn State Milton S. Hershey Medical Center · US

Funding

Translational Research in Lung Biology and DiseaseP30GM103532 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI IRVIN, CHARLES G · 2012 to 2016
$3.7M
Endoplasmic Reticulum Stress Signaling in Allergen-induced Airway RemodelingR01HL122383 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI ANATHY, VIKAS · 2015 to 2023
$3.5M
NHLBI NIH HHS R01 HL122383NIGMS NIH HHS P30 GM103532
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress-induced unfolded protein response plays a critical role in inflammatory diseases, including allergic airway disease. However, the benefits of inhibiting ER stress in the treatment of allergic airway disease are not well known. Herein, we tested the therapeutic potential of a chemical chaperone, tauroursodeoxycholic acid (TUDCA), in combating allergic asthma, using a mouse model of house dust mite (HDM)-induced allergic airway disease. TUDCA was administered during the HDM-challenge phase (preventive regimen), after the HDM-challenge phase (therapeutic regimen), or therapeutically during a subsequent HDM rechallenge (rechallenge regimen). In the preventive regimen, TUDCA significantly decreased HDM-induced inflammation, markers of ER stress, airway hyperresponsiveness (AHR), and fibrosis. Similarly, in the therapeutic regimen, TUDCA administration efficiently decreased HDM-induced airway inflammation, mucus metaplasia, ER stress markers, and AHR, but not airway remodeling. Interestingly, TUDCA administered therapeutically in the HDM rechallenge regimen markedly attenuated HDM-induced airway inflammation, mucus metaplasia, ER stress markers, methacholine-induced AHR, and airway fibrotic remodeling. These results indicate that the inhibition of ER stress in the lungs through the administration of chemical chaperones could be a valuable strategy in the treatment of allergic airway diseases.

Indexed as

Airway RemodelingAnimalsAnti-Asthmatic AgentsAnti-Inflammatory AgentsAsthmaDrug Evaluation, PreclinicalEndoplasmic Reticulum StressFemaleMice, Inbred C57BLPyroglyphidaeRespiratory MucosaTaurochenodeoxycholic AcidAnti-Asthmatic AgentsAnti-Inflammatory AgentsTaurochenodeoxycholic Acidursodoxicoltaurineairway hyperresponsivenessasthmaER stresshouse dust miteinflammation

Identifiers

PMID27154200
PMCPMC4935467
OpenAlexW2347117824

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.