Evidence map›Paper›PMID 24068346›Full record

ArticleCell stress & chaperones2014

TLR2, TLR3, and TLR4 activation specifically alters the oxidative status of intestinal epithelial cells.

Eva Latorre, Carmen Mendoza, Elena Layunta, Ana I Alcalde, José E Mesonero

Open access · bronzeAbstract read
In one paragraph

Article in Cell stress & chaperones, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Eva LatorreDepartment of Pharmacology and Physiology, Faculty of Veterinary Sciences, University of Zaragoza, Miguel Servet 177, 50013, Zaragoza, Spain.
Carmen Mendoza
Elena Layunta
Ana I Alcalde
José E Mesonero
Universidad de Zaragoza · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal inflammatory diseases are the result of multiple processes, including mucosal oxidative stress and perturbed homeostasis between commensal bacteria and mucosal immunity. Toll-like receptors (TLRs) recognize molecular-associated microorganisms' patterns and trigger innate immunity responses contributing to intestinal homeostasis and inflammatory responses. However, TLRs effects on redox balance in intestinal mucosa remain unknown. Therefore, the present study analyzes the effect of TLR2, TLR3, and TLR4 on both oxidative damage of lipids and proteins, and the activity of antioxidant enzymes in enterocyte-like Caco-2 cells. The results show that the activation of these TLRs increased lipid and protein oxidation levels; however, the effect on the antioxidant enzymes activity is different depending on the TLR activated. These results suggest that the activation of TLR2, TLR3, and TLR4 might affect intestinal inflammation by not only their inherent innate immunity responses, but also their pro-oxidative effects on intestinal epithelial cells.

Indexed as

Caco-2 CellsCatalaseEpithelial CellsGlutathione PeroxidaseHumansIntestinal MucosaLipid PeroxidationOxidation-ReductionSuperoxide DismutaseToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like ReceptorsCatalaseGlutathione PeroxidaseSuperoxide DismutaseTLR2 protein, humanTLR3 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID24068346
PMCPMC3933612
OpenAlexW1970158219

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.