Evidence map›Paper›PMID 29805490›Full record

ArticleExperimental and therapeutic medicine2018

Inhibition of microRNA-155 modulates endotoxin tolerance by upregulating suppressor of cytokine signaling 1 in microglia.

Xiaolei Sun, Jie Sun, Xiaoyi Shao, Jinrong Feng, Junming Yan, Yongwei Qin

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Xiaolei SunDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Jie SunDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Xiaoyi ShaoDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Jinrong FengDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Junming YanDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Yongwei QinDepartment of Pathogen Biology and Immunology, Medical College, Nantong University, Nantong, Jiangsu 226001, P.R. China.
Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endotoxin tolerance is an immunohomeostatic reaction to reiterant lipopolysaccharide (LPS) exposure that maintains a state of altered responsiveness in immune cells, resulting in the inhibition of the pro-inflammatory response and the resolution of inflammation. Microglia constitutes the first line of defense against endogenous and external challenges in the brain. MicroRNAs (miRs) serve a critical function in the regulation of inflammation. The aim of the present study was to investigate whether miR-155 regulates endotoxin tolerance. miR-155 and suppressor of cytokine signaling-1 (SOCS1) mRNA expression was measured using RT-qPCR. The expression of SOCS1 was measured by western blotting and immunofluorescence. TNF-α levels were detected by an enzyme-linked immunosorbent assay. The results indicated that miR-155 expression was significantly downregulated in the microglia and cortex tissue following the induction of endotoxin tolerance. This was consistent with an increase in the expression of SOCS1, a predicted target of miR-155 and key inhibitor of the inflammatory reaction. Transfection with miR-155 inhibitor significantly enhanced SOCS1 expression in the microglia following the induction of endotoxin tolerance. SOCS1 knockdown using short hairpin RNA partly inhibited the anti-inflammatory process and promoted the inflammatory response during endotoxin tolerance. The results of the current study indicate that miR-155 inhibition contributes to the development of endotoxin tolerance. Understanding how miRs regulate inflammatory mechanisms may facilitate the development of novel therapeutic strategies to treat CNS disorders.

Indexed as

BV2endotoxin tolerancemicrogliamicroRNA-155suppressor of cytokine signaling 1

Identifiers

PMID29805490
PMCPMC5952101
OpenAlexW2796418807

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.