Evidence map›Paper›PMID 32673430›Full record

ArticleInternational forum of allergy & rhinology2020

Interleukin 13 (IL-13) alters hypoxia-associated genes and upregulates CD73.

Syed Muaz Khalil, Isaac Bernstein, Heather Kulaga, Naina Gour, Nicholas Rowan, Stephane Lajoie, Andrew P Lane

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International forum of allergy & rhinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Ecto-5'-nucleotidase (CD73): an emerging role as prognostic factor in allergic sensitization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. 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

7 authors at 1 institution in 1 country.

Syed Muaz KhalilDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.ORCID 0000-0003-4346-6209
Isaac BernsteinDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.
Heather KulagaDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.
Naina GourThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins School of Medicine, Baltimore, MD.
Nicholas RowanDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.ORCID 0000-0003-1296-2648
Stephane LajoieDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.
Andrew P LaneDepartment of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, MD.ORCID 0000-0001-6369-5469
Johns Hopkins University · US

Funding

Innate Immune Regulation of the Epithelium in Chronic Rhinosinusitis with Nasal PolypsR01AI132590 · NIAID · JOHNS HOPKINS UNIVERSITY · PI LANE, ANDREW P · 2018 to 2022
$3.0M
Dysregulated sensing of invertebrate tropomyosin through dectin-1 confers susceptibility to type-2-mediated allergic diseasesR01AI127644 · NIAID · JOHNS HOPKINS UNIVERSITY · PI LAJOIE, STEPHANE · 2017 to 2021
$2.0M
National Institute of Allergy and Infectious Diseases R01AI132590NIAID NIH HHS R01 AI127644NIAID NIH HHS R01 AI132590
6 · The paper itself

Abstract

backgroundInterleukin 13 (IL-13) is a pleiotropic cytokine that has been shown to be important in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) and other type 2 inflammation-related diseases. Increased IL-13 expression can elicit several pro-inflammatory effects, including eosinophilia, and pathology such as increased mucus secretion. Polypogenesis in chronic rhinosinusitis (CRS) can be caused by hypoxia, which can also lead to hyperpermeability of airway epithelium and epithelium-to-mesenchymal translation through the upregulation of hypoxia-associated genes, such as HIF1. Whether T-helper 2 (Th2) inflammatory cytokines, such as IL-13, can also induce sinonasal epithelial hypoxia-associated genes is currently unknown.

methodsHuman air-liquid interface (ALI) sinonasal epithelial cell cultures treated with recombinant IL-13 were analyzed by real-time polymerase chain reaction (PCR) and flow cytometry to determine the effect on epithelial cells.

resultsWhole tissue from CRSwNP subjects showed increased HIF1A gene expression. Treatment of fully differentiated human ALI cultures with IL-13 resulted in a concurrent increase in HIF1A and ARNT messenger RNA (mRNA) expression. However, the level of EPAS1 expression was significantly reduced. IL-13 also had a dose-dependent response on the expression of HIF genes and the time course experiment showed peak expression of HIF1A and ARNT at 5 to 7 days poststimulation. Remarkably, CD73 surface expression also peaked at day 5 poststimulation.

conclusionOur data suggests that IL-13 can induce hypoxia signaling pathway genes leading to surface expression of CD73, which has an anti-inflammatory effect.

Indexed as

Nasal PolypsRhinitisSinusitisChronic DiseaseEpithelial CellsHumansHypoxiaInterleukin-13Interleukin-33Nasal MucosaInterleukin-13Interleukin-33CD73cell culturehypoxiaIL-13sinonasal epithelium

Identifiers

PMID32673430
PMCPMC11268491
OpenAlexW3043767362

What OpenQuestion holds

Textmetadata
LicenceTDM
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.