Evidence map›Paper›PMID 21674728›Full record

ArticleInflammatory bowel diseases2012

Wnt2 inhibits enteric bacterial-induced inflammation in intestinal epithelial cells.

Xingyin Liu, Rong Lu, Shaoping Wu, Yong-Guo Zhang, Yinglin Xia, R Balfour Sartor, Jun Sun

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. A Protective Role of Canonical Wnt/Mediators of inflammation · 2024
    Review
  5. Review
  6. Speaking the host language: howMicrobiology (Reading, England) · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. An update on Wnt signaling pathway in cancer.Translational cancer research · 2020
    Review
  14. Oral and intestinal bacterial exotoxins: Potential linked to carcinogenesis.Progress in molecular biology and translational science · 2020
    Review
  15. Article
  16. Diseases (Basel, Switzerland) · 2019
    Review
  17. Review
  18. Review
  19. Article
  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

7 authors at 2 institutions in 1 country.

Xingyin LiuGastroenterology & Hepatology Division, Department of Medicine, University of Rochester, Rochester, New York, North Carolina, USA.
Rong Lu
Shaoping Wu
Yong-Guo Zhang
Yinglin Xia
R Balfour Sartor
Jun Sun
University of Rochester · USUniversity of North Carolina at Chapel Hill · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
Colitis Induced by immune responses to luminal bacteria-mouseR01DK053347 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 1998 to 2012
$4.6M
NATIONAL GNOTOBIOTIC RODENT RESOURCE CENTER: AIDSP40RR018603 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SARTOR, RYAN B · 2004 to 2011
$4.0M
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
NCRR NIH HHS P40 RR018603NIDDK NIH HHS DK075386-0251NIDDK NIH HHS K01 DK075386NIDDK NIH HHS NIHR01 DK053347NIDDK NIH HHS P30 DK034987NIDDK NIH HHS R03 DK089010NIDDK NIH HHS R03DK089010-01
6 · The paper itself

Abstract

backgroundWnt signaling plays an essential role in gastrointestinal epithelial proliferation. Most investigations have focused on developmental and immune responses. Bacterial infection can be chronic and increases the risk of inflammatory bowel disease and colitis-associated cancer. However, we lack studies on how bacteria regulate Wnt proteins and how Wnts modulate the host responses to enteric bacteria. This study investigated the effects of Salmonella and Escherichia coli on Wnt2, one of the Wnt family members, in intestinal epithelia cells.

methodsUsing cultured epithelial cells, a Salmonella-colitis mouse model, and a gnotobiotic mouse model, we found that Wnt2 mRNA and protein expression levels were elevated after bacterial infection. Enteric bacteria regulate Wnt2 location in the intestine. Furthermore, we found that elevation of Wnt2 was a strategy for host defense by inhibiting cell apoptosis and inflammatory responses to infection.

resultsUsing Wnt2 siRNA analysis, we show enhanced inflammatory cytokine IL-8 in epithelial cells. Cells overexpressed Wnt2 had less bacterial-induced IL-8 secretion. AvrA is a bacterial protein that inhibits inflammation by stabilizing β-catenin, the downstream target of Wnt. We found that the stabilization of Wnt2 was regulated through ubiquitination. Moreover, the bacterial protein AvrA from Salmonella and E. coli stabilized Wnt2 protein expression in vivo. In an ex-germ-free system, E. coli F18 expressing AvrA increased Wnt2 expression and changed Wnt2 distribution in intestine.

conclusionsWnt2 contributes to host protection in response to enteric bacteria. Our findings thus reveal a previously undefined role of Wnt for host-pathogen interaction and inflammation.

Indexed as

AnimalsApoptosisBacterial ProteinsCells, CulturedColitisEpithelial CellsEscherichia coli InfectionsHost-Pathogen InteractionsInterleukin-8Intestinal MucosaMiceRNA, MessengerRNA, Small InterferingSalmonella InfectionsSalmonella typhimuriumUbiquitinationAvrA protein, Salmonella typhimuriumBacterial ProteinsInterleukin-8RNA, MessengerRNA, Small InterferingWnt2 Protein

Identifiers

PMID21674728
PMCPMC3294455
OpenAlexW2133240270

What OpenQuestion holds

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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.