Evidence map›Paper›PMID 21078560›Full record

ArticleCytokine2011

Facultative heterochromatin formation at the IL-1 beta promoter in LPS tolerance and sepsis.

Barbara K Yoza, Charles E McCall

Abstract read
In one paragraph

Article in Cytokine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Histone Lys demethylase KDM3C demonstrates anti-inflammatory effects by suppressing NF-κB signaling and osteoclastogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  7. Review
  8. Review
  9. Sirtuins and Immuno-Metabolism of Sepsis.International journal of molecular sciences · 2018
    Review
  10. Interleukin-1 Beta-A Friend or Foe in Malignancies?International journal of molecular sciences · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. RelB: an outlier in leukocyte biology.Journal of leukocyte biology · 2013
    Review
  17. Article
  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

2 authors at 1 institution in 1 country.

Barbara K YozaDepartment of Surgery, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157, USA. byoza@wfubmc.edu
Charles E McCall
Wake Forest University · US

Funding

WORKER PROTECTION AGAINST AIRBORNE INFLUENZA - A PILOT STUDYM01RR007122 · NCRR · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOLMES, ROSS P · 1992 to 2010
$35.2M
NF-kB and Chromatin Changes in Human SepsisR01AI065791 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCALL, CHARLES EMORY · 2006 to 2015
$4.3M
Epigenetics of Severe Systemic InflammationR01AI079144 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCALL, CHARLES EMORY · 2010 to 2014
$2.0M
FUNCTIONAL AND METABOLIC PROPERTIES OF TOXIC NEUTROPHILSR01AI009169 · NIAID · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCALL, CHARLES EMORY · 1985 to 2003
$1.3M
NCRR NIH HHS M01 RR007122NCRR NIH HHS MO-1RR 007122NIAID NIH HHS R01 AI009169NIAID NIH HHS R01 AI065791NIAID NIH HHS R01AI-065791NIAID NIH HHS R01 AI079144NIAID NIH HHS R01AI-079144NIAID NIH HHS R01AI-09169
6 · The paper itself

Abstract

The clinical phenotype in sepsis that is observed as LPS tolerance is determined by silencing of pro-inflammatory genes like IL-1 beta (IL-1β). This study shows that facultative heterochromatin (fHC) silences IL-1β expression during sepsis, where we find dephosphorylated histone H3 serine 10 and increased binding of heterochromatin protein-1 (HP-1) to the promoter. In both human sepsis blood leukocytes and an LPS tolerant human THP-1 cell model, we show that IκBα and v-rel reticuloendotheliosis viral oncogene homolog B (RelB) function as dominant labile mediators of fHC formation at the IL-1β promoter. Protein synthesis inhibition decreases levels of IκBα and RelB, converts silent fHC to euchromatin, and restores IL-1β transcription. We further show TLR dependent NFκB p65 and histone H3 serine 10 phosphorylation binding at the promoter. We conclude that the resolution phase of sepsis, which correlates with survival in humans, may depend on the plasticity of chromatin structure as found in fHC.

Indexed as

AdultAgedFemaleHeterochromatinHistonesHumansI-kappa B ProteinsImmune ToleranceInterleukin-1betaLipopolysaccharidesMaleMiddle AgedModels, ImmunologicalNF-KappaB Inhibitor alphaPhosphorylationPromoter Regions, GeneticHeterochromatinHistonesI-kappa B ProteinsInterleukin-1betaLipopolysaccharidesNF-KappaB Inhibitor alphaNFKBIA protein, humanTranscription Factor RelATranscription Factor RelB

Identifiers

PMID21078560
PMCPMC3021647
OpenAlexW2059997982

What OpenQuestion holds

Textmetadata
LicenceTDM
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.