Evidence map›Paper›PMID 21303908›Full record

ArticleThe Journal of biological chemistry2011

Interleukin-13 (IL-13)/IL-13 receptor alpha1 (IL-13Ralpha1) signaling regulates intestinal epithelial cystic fibrosis transmembrane conductance regulator channel-dependent Cl- secretion.

David Wu, Richard Ahrens, Heather Osterfeld, Taeko K Noah, Katherine Groschwitz, Paul S Foster, Kris A Steinbrecher, Marc E Rothenberg, Noah F Shroyer, Klaus I Matthaei and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Tuft cell-derived acetylcholine regulates epithelial fluid secretion.bioRxiv : the preprint server for biology · 2023
    Article
  6. Article
  7. Goblet cell hyperplasia is not epithelial-autonomous in the Cftr knockout intestine.American journal of physiology. Gastrointestinal and liver physiology · 2022
    Article
  8. Article
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  16. Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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  18. Article
  19. Review
  20. 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

12 authors at 4 institutions in 3 countries.

David WuDivision of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.
Richard Ahrens
Heather Osterfeld
Taeko K Noah
Katherine Groschwitz
Paul S Foster
Kris A Steinbrecher
Marc E Rothenberg
Noah F Shroyer
Klaus I Matthaei
Fred D Finkelman
Simon P Hogan
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · USKing Saud University · SAUniversity of Newcastle Australia · AU

Funding

The role of ATOH1 as a tumor suppressor in colorectal cancerR01CA142826 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI SHROYER, NOAH FREEMAN · 2010 to 2014
$1.5M
Interleukin-9 In Experimental Intestinal AnaphylaxisR01AI073553 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HOGAN, SIMON PATRICK · 2008 to 2011
$1.5M
SPDEF in intestinal differentiation.R03DK084167 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI SHROYER, NOAH FREEMAN · 2009 to 2010
$151k
NCI NIH HHS R01 CA142826NIAID NIH HHS R01 AI073553NIAID NIH HHS R01AI073553-01NIDDK NIH HHS R03 DK084167
6 · The paper itself

Abstract

Interleukin-13 (IL-13) has been linked to the pathogenesis of inflammatory diseases of the gastrointestinal tract. It is postulated that IL-13 drives inflammatory lesions through the modulation of both hematopoietic and nonhematopoietic cell function in the intestine. To delineate the relevant contribution of elevated levels of intestinal IL-13 to intestinal structure and function, we generated an intestinal IL-13 transgenic mouse (iIL-13Tg). We show that constitutive overexpression of IL-13 in the small bowel induces modification of intestinal epithelial architecture (villus blunting, goblet cell hyperplasia, and increased epithelial proliferation) and epithelial function (altered basolateral → apical Cl(-) ion conductance). Pharmacological analyses in vitro and in vivo determined that elevated Cl(-) conductance is mediated by altered cystic fibrosis transmembrane conductance regulator expression and activity. Generation of iIL-13Tg/Il13rα1(-/-), iIL-13Tg/Il13rα2(-/-), and iIL-13Tg/Stat6(-/-) mice revealed that IL-13-mediated dysregulation of epithelial architecture and Cl(-) conductance is dependent on IL-13Rα1 and STAT-6. These observations demonstrate a central role for the IL-13/IL-13Rα1 pathway in the regulation of intestinal epithelial cell Cl(-) secretion via up-regulation of cystic fibrosis transmembrane conductance regulator, suggesting an important role for this pathway in secretory diarrhea.

Indexed as

AnimalsCaco-2 CellsChloridesCystic Fibrosis Transmembrane Conductance RegulatorCystsDiarrheaFibrosisHumansInterleukin-13Interleukin-13 Receptor alpha1 SubunitIntestinal DiseasesIntestinal MucosaIon TransportMiceMice, Inbred BALB CMice, KnockoutChloridesCystic Fibrosis Transmembrane Conductance RegulatorIl13ra1 protein, mouseInterleukin-13Interleukin-13 Receptor alpha1 SubunitStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID21303908
PMCPMC3075682
OpenAlexW2073471607

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.