Evidence map›Paper›PMID 18678662›Full record

ArticleInfection and immunity2008

Tumor suppressor Foxo3a is involved in the regulation of lipopolysaccharide-induced interleukin-8 in intestinal HT-29 cells.

Lobke Snoeks, Christopher R Weber, Jerrold R Turner, Mitra Bhattacharyya, Kaarin Wasland, Suzana D Savkovic

Abstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. FOXO3: at the crossroads of metabolic, inflammatory, and tumorigenic remodeling in the colon.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Review
  4. Toxins · 2023
    Article
  5. mBio · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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  12. Article
  13. Article
  14. Review
  15. Reduced mitochondrial activity in colonocytes facilitates AMPKα2-dependent inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  16. Article
  17. Intestinal inflammation requires FOXO3 and prostaglandin E2-dependent lipogenesis and elevated lipid droplets.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Article
  18. Article
  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

6 authors at 2 institutions in 1 country.

Lobke SnoeksDepartment of Medicine, Division of Gastroenterology, Evanston-Northwestern Research Institute, Evanston, Illinois 60201, USA.
Christopher R Weber
Jerrold R Turner
Mitra Bhattacharyya
Kaarin Wasland
Suzana D Savkovic
Western Research Institute · USUniversity of Chicago · US

Funding

Mechanisms of epithelial barrier dysfunction mediated by inflammatory cytokinesF32DK082134 · NIDDK · UNIVERSITY OF CHICAGO · PI WEBER, CHRISTOPHER · 2008 to 2009
$108k
NIDDK NIH HHS F32 DK082134NIDDK NIH HHS F32DK082134
6 · The paper itself

Abstract

Enteric bacteria and their products play an important role in intestinal inflammation; however, the complete mechanisms are not elucidated yet. Tumor suppressor Foxo3a regulates gene expression in the nucleus, and its translocation to the cytosol leads to inactivation. Proximally, Foxo3a is regulated by different pathways including the phosphoinositide 3-kinase (PI3K) pathway. The aim of this study was to determine the effect of bacterial infection on Foxo3a in intestinal epithelial cells and to examine the contribution of Foxo3a in intestinal inflammation. Bacterial lipopolysaccharide (LPS) and infection with mouse pathogen Citrobacter rodentium induce translocation of the nuclear Foxo3a into the cytosol, where it degrades in human HT-29 and mouse CMT-93 cells. In colonic epithelia of healthy mice, Foxo3a is localized in the epithelia at the bottom of the crypts in both the nucleus and the cytosol, while in C. rodentium-infected colon Foxo3a is expressed along the crypts and located mainly in the cytosol, suggesting its inactivation. LPS utilized the PI3K pathway to inhibit Foxo3a. Additionally, inhibition of PI3K attenuated LPS-induced proinflammatory interleukin-8 (IL-8). LPS-induced IL-8 is increased in HT-29 cells with silenced Foxo3a. Moreover, in HT-29 cells with silenced Foxo3a, the amount of IkappaBalpha, an NF-kappaB inhibitor, is decreased. In conclusion, LPS and bacterial infection inactivate Foxo3a in intestinal epithelia via the PI3K pathway and inactivated Foxo3a leads to the upregulation of IL-8 by suppressing inhibitory IkappaBalpha.

Indexed as

AnimalsCitrobacter rodentiumColonEpithelial CellsForkhead Box Protein O3Forkhead Transcription FactorsHT29 CellsHumansInterleukin-8Intestinal MucosaLipopolysaccharidesMiceMice, Inbred C57BLModels, BiologicalPhosphatidylinositol 3-KinasesCXCL8 protein, humanForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, humanFoxO3 protein, mouseInterleukin-8LipopolysaccharidesPhosphatidylinositol 3-Kinases

Identifiers

PMID18678662
PMCPMC2546851
OpenAlexW2135757563

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.