Evidence map›Paper›PMID 31955243›Full record

ArticleCellular and molecular life sciences : CMLS2020

Epigenetic histone modulation contributes to improvements in inflammatory bowel disease via EBI3.

Alexandra Wetzel, Bettina Scholtka, Christian Gerecke, Burkhard Kleuser

Open access · hybridAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. 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
1.1field-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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Histone deacetylase in inflammatory bowel disease: novel insights.Therapeutic advances in gastroenterology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Epigenetics of Inflammatory Bowel Diseases.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Epigenetic DNA Methylation ofInternational journal of molecular sciences · 2021
    Article
  18. Review
  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

4 authors at 1 institution in 1 country.

Alexandra WetzelDepartment of Nutritional Toxicology, Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
Bettina ScholtkaDepartment of Nutritional Toxicology, Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
Christian GereckeDepartment of Nutritional Toxicology, Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany.
Burkhard KleuserDepartment of Nutritional Toxicology, Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-Allee 114-116, 14558, Nuthetal, Germany. kleuser@uni-potsdam.de.
University of Potsdam · DE

Funding

Bundesministerium für Bildung und Forschung 01EA1408A-BDeutsche Forschungsgemeinschaft GRK 2098
6 · The paper itself

Abstract

Ulcerative colitis (UC) is characterized by relapsing-remitting inflammatory episodes paralleled by varying cytokine levels, suggesting that switching epigenetic processes might be involved. However, the epigenetic impact on cytokine levels in colitis is mostly unexplored. The heterodimeric interleukin (IL)-12 cytokine family have various functions in both pro- and anti-inflammatory processes. The family member IL-35 (EBI3/IL-12p35) was recently reported to play an anti-inflammatory role in UC. Therefore, we aimed to investigate a possible epigenetic regulation of the IL-35 subunits in vitro and in vivo, and to examine the epigenetic targeting of EBI3 expression as a therapeutic option for UC. Exposure to either the pro-inflammatory TNFα or to histone deacetylase inhibitors (HDACi) significantly increased EBI3 expression in Human Colon Epithelial Cells (HCEC) generated from healthy tissue. When applied in combination, a drastic upregulation of EBI3 expression occurred, suggesting a synergistic mechanism. Consequently, IL-35 was increased as well. In vivo, the intestines of HDACi-treated wild-type mice exhibited reduced pathological signs of colitis compared to non-treated colitic mice. However, the improvement by HDACi treatment was completely lost in Ebi3-deficient mice (Ebi3

Indexed as

Epigenesis, GeneticAnimalsCaspase 3CD3 ComplexColitisDextran SulfateHistone Deacetylase InhibitorsHistonesHumansInflammationInflammatory Bowel DiseasesInterleukin-12InterleukinsMice, Inbred C57BLMinor Histocompatibility AntigensPhenotypeCaspase 3CD3 ComplexDextran SulfateEBI3 protein, humanEbi3 protein, mouseHistone Deacetylase InhibitorsHistonesInterleukin-12InterleukinsMinor Histocompatibility AntigensReceptors, CytokineTumor Necrosis Factor-alphaVorinostatHistone deacetylase inhibitorInhibitory cytokinesInterleukin-35SAHAUlcerative colitis

Identifiers

PMID31955243
PMCPMC7658076
OpenAlexW3000125435

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.