Evidence map›Paper›PMID 35608904›Full record

ArticleJCI insight2022

IL-13-programmed airway tuft cells produce PGE2, which promotes CFTR-dependent mucociliary function.

Maya E Kotas, Camille M Moore, Jose G Gurrola, Steven D Pletcher, Andrew N Goldberg, Raquel Alvarez, Sheyla Yamato, Preston E Bratcher, Ciaran A Shaughnessy, Pamela L Zeitlin and 8 more

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

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

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  18. G protein subunit GeLife · 2024
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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

18 authors at 5 institutions in 1 country.

Maya E KotasDivision of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Camille M MooreCenter for Genes, Environment, and Health, National Jewish Health, Denver, Colorado, USA.
Jose G GurrolaDepartment of Otolaryngology - Head and Neck Surgery, University of California, San Francisco, San Francisco, California, USA.
Steven D PletcherDepartment of Otolaryngology - Head and Neck Surgery, University of California, San Francisco, San Francisco, California, USA.
Andrew N GoldbergDepartment of Otolaryngology - Head and Neck Surgery, University of California, San Francisco, San Francisco, California, USA.
Raquel AlvarezDivision of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Sheyla YamatoDivision of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
Preston E BratcherDepartment of Pediatrics, National Jewish Health, Denver, Colorado, USA.
Ciaran A ShaughnessyDepartment of Pediatrics, National Jewish Health, Denver, Colorado, USA.
Pamela L ZeitlinDepartment of Pediatrics, National Jewish Health, Denver, Colorado, USA.
Irene H ZhangCenter for Applied Microbiome Sciences, Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, Arizona, USA.
Yingchun LiCenter for Genes, Environment, and Health, National Jewish Health, Denver, Colorado, USA.
Michael T MontgomeryCenter for Genes, Environment, and Health, National Jewish Health, Denver, Colorado, USA.
Keehoon LeeCenter for Applied Microbiome Sciences, Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, Arizona, USA.
Emily K CopeCenter for Applied Microbiome Sciences, Pathogen and Microbiome Institute, Northern Arizona University, Flagstaff, Arizona, USA.
Richard M LocksleyHoward Hughes Medical Institute and.
Max A SeiboldCenter for Genes, Environment, and Health, National Jewish Health, Denver, Colorado, USA.
Erin D GordonDivision of Pulmonary, Critical Care, Allergy and Sleep Medicine, Department of Medicine, University of California, San Francisco, San Francisco, California, USA.
National Jewish Health · USUniversity of California, San Francisco · USNorthern Arizona University · USHoward Hughes Medical Institute · USSan Francisco VA Medical Center · US

Funding

Role of miRNAs in Th2-Driven inflammation in AsthmaP01HL107202 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 2012 to 2023
$23.3M
Parasite immunity orchestrated by type 2 immune cellsR01AI026918 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 1988 to 2022
$3.8M
Understanding the Molecular Genetic Mechanisms of Asthma Risk Loci: IL33, IL1RL1, and GSDMB - COVID 19 SupplementR01AI136962 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GORDON, ERIN D. · 2018 to 2022
$3.4M
Mentoring Research in Precision Medicine for Lung DiseaseK24HL137013 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PRESCOTT G WOODRUFF · 2017 to 2026
$1.2M
Determining the Role of the Upper and Lower Airway Microbiota as Drivers of Concomitant Inflammatory Responses in patients with Chronic Rhinosinusitis and AsthmaR15AI147148 · NIAID · NORTHERN ARIZONA UNIVERSITY · PI CAPORASO, JAMES GREGORY, COPE, EMILY K · 2019 to 2019
$468k
NHLBI NIH HHS K24 HL137013NHLBI NIH HHS P01 HL107202NIAID NIH HHS R01 AI026918NIAID NIH HHS R01 AI136962NIAID NIH HHS R15 AI147148
6 · The paper itself

Abstract

Chronic type 2 (T2) inflammatory diseases of the respiratory tract are characterized by mucus overproduction and disordered mucociliary function, which are largely attributed to the effects of IL-13 on common epithelial cell types (mucus secretory and ciliated cells). The role of rare cells in airway T2 inflammation is less clear, though tuft cells have been shown to be critical in the initiation of T2 immunity in the intestine. Using bulk and single-cell RNA sequencing of airway epithelium and mouse modeling, we found that IL-13 expanded and programmed airway tuft cells toward eicosanoid metabolism and that tuft cell deficiency led to a reduction in airway prostaglandin E2 (PGE2) concentration. Allergic airway epithelia bore a signature of PGE2 activation, and PGE2 activation led to cystic fibrosis transmembrane receptor-dependent ion and fluid secretion and accelerated mucociliary transport. These data reveal a role for tuft cells in regulating epithelial mucociliary function in the allergic airway.

Indexed as

Cystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorAnimalsDinoprostoneInterleukin-13MiceRespiratory SystemCystic Fibrosis Transmembrane Conductance RegulatorDinoprostoneInterleukin-13AllergyChloride channelsEicosanoidsInflammationPulmonology

Identifiers

PMID35608904
PMCPMC9310525
OpenAlexW4281382047

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.