Evidence map›Paper›PMID 23822876›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

Foxa2 regulates leukotrienes to inhibit Th2-mediated pulmonary inflammation.

Xiaoju Tang, Xiaojing J Liu, Cuijie Tian, Qiaoli Su, Yi Lei, Qingbo Wu, Yangyan He, Jeffrey A Whitsett, Fengming Luo

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Epigenetic Approaches to Identifying Asthma Endotypes.Allergy, asthma & immunology research · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. An Elusive Fox that Suppresses Scgb1a1 in Asthma Has Been Found.American journal of respiratory cell and molecular biology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

9 authors at 4 institutions in 3 countries.

Xiaoju Tang1 Research Center of Regeneration Medicine.
Xiaojing J Liu
Cuijie Tian
Qiaoli Su
Yi Lei
Qingbo Wu
Yangyan He
Jeffrey A Whitsett
Fengming Luo
Sichuan University · CNCincinnati Children's Hospital Medical Center · USPulmonary Associates · USTissue Regeneration Systems (United States) · US

Funding

Transcriptional Programming of Asthma Related Pathology in Respiratory EpitheliaR01HL095580 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WHITSETT, JEFFREY A · 2009 to 2017
$4.7M
Transcriptional Control of Submucosal Gland Formation and FunctionR01HL108907 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WHITSETT, JEFFREY A · 2011 to 2014
$1.6M
NHLBI NIH HHS HL095580NHLBI NIH HHS R01 HL095580NHLBI NIH HHS R01 HL108907
6 · The paper itself

Abstract

Foxa2 is a member of the Forkhead family of nuclear transcription factors that is highly expressed in respiratory epithelial cells of the developing and mature lung. Foxa2 is required for normal airway epithelial differentiation, and its deletion causes goblet-cell metaplasia and Th2-mediated pulmonary inflammation during postnatal development. Foxa2 expression is inhibited during aeroallergen sensitization and after stimulation with Th2 cytokines, when its loss is associated with goblet-cell metaplasia. Mechanisms by which Foxa2 controls airway epithelial differentiation and Th2 immunity are incompletely known. During the first 2 weeks after birth, the loss of Foxa2 increases the production of leukotrienes (LTs) and Th2 cytokines in the lungs of Foxa2 gene-targeted mice. Foxa2 expression inhibited 15-lipoxygenase (Alox15) and increased Alox5 transcription, each encoding key lipoxygenases associated with asthma. The inhibition of the cysteinyl LT (CysLT) signaling pathway by montelukast inhibited IL-4, IL-5, eotaxin-2, and regulated upon activation normal T cell expressed and presumably secreted expression in the developing lungs of Foxa2 gene-targeted mice. Montelukast inhibited the expression of genes regulating mucus metaplasia, including Spdef, Muc5ac, Foxa3, and Arg2. Foxa2 plays a cell-autonomous role in the respiratory epithelium, and is required for the suppression of Th2 immunity and mucus metaplasia in the developing lung in a process determined in part by its regulation of the CysLT pathway.

Indexed as

AcetatesAnimalsArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseArachidonate 5-LipoxygenaseCyclopropanesCysteineDisease Models, AnimalEosinophilsGoblet CellsHepatocyte Nuclear Factor 3-betaInflammation MediatorsLeukotriene AntagonistsLeukotrienesMetaplasiaMiceAcetatesAlox15 protein, mouseArachidonate 12-LipoxygenaseArachidonate 15-LipoxygenaseArachidonate 5-LipoxygenaseCyclopropanesCysteinecysteinyl-leukotrieneFoxa2 protein, mouseHepatocyte Nuclear Factor 3-betaInflammation MediatorsLeukotriene AntagonistsLeukotrienesmontelukastQuinolinesSulfides

Identifiers

PMID23822876
PMCPMC3931118
OpenAlexW2092712258

What OpenQuestion holds

Textmetadata
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.