Evidence map›Paper›PMID 26498350›Full record

ArticleOncotarget2015

Hepatic TLR4 signaling is activated by LPS from digestive tract during SARA, and epigenetic mechanisms contribute to enforced TLR4 expression.

Guangjun Chang, Su Zhuang, Hans-Martin Seyfert, Kai Zhang, Tianle Xu, Di Jin, Junfei Guo, Xiangzhen Shen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-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

22 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Targeting gut microbiota as a possible therapy for mastitis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2019
    Review
  14. Article
  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

8 authors at 2 institutions in 2 countries.

Guangjun ChangCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Su ZhuangCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Hans-Martin SeyfertLeibniz Institute for Farm Animal Biology, Dummerstorf, Germany.
Kai ZhangCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Tianle XuCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Di JinCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Junfei GuoCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Xiangzhen ShenCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Nanjing Agricultural University · CNResearch Institute for Farm Animal Biology (FBN) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subacute ruminal acidosis (SARA) is known to trigger a systemic inflammatory response that is possibly caused by the translocation of lipopolysaccharides (LPS) from the gastrointestinal tract into the bloodstream. The aim of this study is to investigate this causal relationship between the increases of circulating LPS and liver inflammation. Here we found that SARA goats exhibited significantly increased LPS concentrations in both the rumen and portal vein. The livers of these goats exhibited increased mRNA concentrations of pro-inflammatory genes that indicated inflammation. Meanwhile, the occurrence of liver inflammation was further validated by the enhanced protein expression of those cytokines in the livers of SARA goats. These increased expressions of detected pro-inflammatory genes were likely mediated by enforced TLR4 signaling because SARA increased the concentrations of TLR4 mRNA and protein in the liver and the abundance of both the NF-kB-p65 factor and its active phosphorylated variant. We also verified that the enhanced TLR4 expression was accompanied by chromatin decompaction and demethylation of the proximal TLR4 promoter. Hence, epigenetic mechanisms are involved in the enforced expression of immune genes during SARA, and these findings open innovative routes for interventions via the modulation of these epigenetic mechanisms.

Indexed as

AcidosisAnimalsCattleEpigenesis, GeneticGastrointestinal TractGoat DiseasesGoatsHepatitisLipopolysaccharidesRumenSignal TransductionToll-Like Receptor 4LipopolysaccharidesToll-Like Receptor 4epigenetic mechanismsImmune responseImmunityImmunology and Microbiology SectionliverLPS translocationsubacute ruminal acidosisTLR4 signaling

Identifiers

PMID26498350
PMCPMC4770722
OpenAlexW2191339667

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.