Evidence map›Paper›PMID 33815402›Full record

ArticleFrontiers in immunology2021

The Protective Effects of IL-31RA Deficiency During Bleomycin-Induced Pulmonary Fibrosis.

Dan J K Yombo, Varshini Odayar, Nishant Gupta, Anil G Jegga, Satish K Madala

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. 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
2.8field-weighted citation impact, top 9% 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, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Highlights on Future Treatments of IPF: Clues and Pitfalls.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023
    Review
  11. Article
  12. Review
  13. Review
  14. 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

5 authors at 3 institutions in 1 country.

Dan J K YomboDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Varshini OdayarDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
Nishant GuptaDivision of Pulmonary, Critical Care and Sleep Medicine, University of Cincinnati, Cincinnati, OH, United States.
Anil G JeggaDepartment of Pediatrics, College of Medicine, University of Cincinnati, Cincinnati, OH, United States.
Satish K MadalaDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States.
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

WT1 REGULATION OF PULMONARY FIBROSISR01HL134801 · NHLBI · UNIVERSITY OF CINCINNATI · PI MADALA, SATISH K · 2017 to 2025
$3.9M
Sox9 Regulation of Fibroblast Activation and Pulmonary FibrosisR01HL157176 · NHLBI · UNIVERSITY OF CINCINNATI · PI MADALA, SATISH K · 2021 to 2025
$2.5M
IL-31 Regulation of Immunopathology in Pulmonary FibrosisR21AG059533 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI MADALA, SATISH K · 2018 to 2019
$452k
NHLBI NIH HHS R01 HL134801NHLBI NIH HHS R01 HL157176NIA NIH HHS R21 AG059533
6 · The paper itself

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a severe fibrotic lung disease characterized by excessive collagen deposition and progressive decline in lung function. Th2 T cell-derived cytokines including IL-4 and IL-13 have been shown to contribute to inflammation and fibrotic remodeling in multiple tissues. Interleukin-31 (IL-31) is a newly identified cytokine that is predominantly produced by CD4 Th2 T cells, but its signaling receptor IL-31RA is primarily expressed by non-hematopoietic cells. However, the potential role of the IL-31-IL31RA axis in pulmonary inflammation and fibrosis has remained largely unknown. To determine the role of IL-31RA deficiency in pulmonary fibrosis, wildtype, and IL-31RA knockout mice were treated with bleomycin and measured changes in collagen deposition and lung function. Notably, the loss of IL-31 signaling attenuated collagen deposition and lung function decline during bleomycin-induced pulmonary fibrosis. The total lung transcriptome analysis showed a significant reduction in fibrosis-associated gene transcripts including extracellular matrix and epithelial cell-associated gene networks. Furthermore, the lungs of human IPF showed an elevated expression of IL-31 when compared to healthy subjects. In support, the percentage of IL-31 producing CD4

Indexed as

AnimalsBleomycinCollagenFemaleIdiopathic Pulmonary FibrosisInterleukinsLungMaleMiceMice, Inbred C57BLReceptors, InterleukinBleomycinCollagenIl31ra protein, mouseinterleukin-31, mouseInterleukinsReceptors, Interleukinbleomycin IL-31 regulation of pulmonary fibrosisidiopathic pulmonary fibrosisinterleukin 31interleukin 31 receptor alphalung

Identifiers

PMID33815402
PMCPMC8017338
OpenAlexW3138969259

What OpenQuestion holds

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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.