Evidence map›Paper›PMID 21903761›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011

Wingless homolog Wnt11 suppresses bacterial invasion and inflammation in intestinal epithelial cells.

Xingyin Liu, Shaoping Wu, Yinglin Xia, Xi Emma Li, Yuxuan Xia, Zhongren David Zhou, Jun Sun

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. A Protective Role of Canonical Wnt/Mediators of inflammation · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Oral and intestinal bacterial exotoxins: Potential linked to carcinogenesis.Progress in molecular biology and translational science · 2020
    Review
  14. Review
  15. Article
  16. Article
  17. Diseases (Basel, Switzerland) · 2019
    Review
  18. Article
  19. Review
  20. 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 2 institutions in 1 country.

Xingyin LiuGastroenterology & Hepatology Division, Department of Medicine, University of Rochester, Rochester, New York 14642, USA.
Shaoping Wu
Yinglin Xia
Xi Emma Li
Yuxuan Xia
Zhongren David Zhou
Jun Sun
University of Rochester · USBrighton Hospital · US

Funding

NF-kB /Beta-catenin interaction during intestinal inflammationK01DK075386 · NIDDK · UNIVERSITY OF ROCHESTER · PI SUN, JUN · 2007 to 2011
$651k
Enteric bacterial modulation of Vitamin D Receptor signaling in colitisR03DK089010 · NIDDK · UNIVERSITY OF ROCHESTER · PI SUN, JUN · 2010 to 2011
$154k
NIDDK NIH HHS DK-075386-0251NIDDK NIH HHS K01 DK075386NIDDK NIH HHS R03 DK089010NIDDK NIH HHS R03DK-089010-01
6 · The paper itself

Abstract

Wnt11 plays an essential role in gastrointestinal epithelial proliferation, and previous investigations have focused on development and immune responses. However, the roles of how enteric bacteria regulate Wnt11 and how Wnt11 modulates the host response to pathogenic bacteria remain unexplored. This study investigated the effects of Salmonella infection on Wnt activation in intestinal epithelial cells. We found that Wnt11 mRNA and protein expression were elevated after Salmonella colonization. Wnt11 protein secretion in epithelial cells was also elevated after bacterial infection. Furthermore, we demonstrated that pathogenic Salmonella regulated Wnt11 expression and localization in vivo. We found a decrease in Salmonella invasion in cells with Wnt11 overexpression compared with cells with normal Wnt11 level. IL-8 mRNA in Wnt11-transfected cells was low; however, it was enhanced in cells with a low level of Wnt11 expression. Functionally, Wnt11 overexpression inhibited Salmonella-induced apoptosis. AvrA is a known bacterial effector protein that stabilizes β-catenin, the downstream regulator of Wnt signaling, and inhibits bacterially induced intestinal inflammation. We observed that Wnt11 expression, secretion, and transcriptional activity were regulated by Salmonella AvrA. Overall, Wnt11 is involved in the protection of the host intestinal cells by blocking the invasion of pathogenic bacteria, suppressing inflammation, and inhibiting apoptosis. Wnt11 is a novel and important contributor to intestinal homeostasis and host defense.

Indexed as

AnimalsApoptosisBacterial Proteinsbeta CateninCaco-2 CellsColonDisease Models, AnimalEpithelial CellsFemaleGene ExpressionHT29 CellsHumansMiceMice, Inbred C57BLSalmonella InfectionsSalmonella typhimuriumAvrA protein, Salmonella typhimuriumBacterial Proteinsbeta CateninWnt11 protein, humanWnt11 protein, mouseWnt Proteins

Identifiers

PMID21903761
PMCPMC3233790
OpenAlexW2148999014

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.