Evidence map›Paper›PMID 30153074›Full record

ArticleCell cycle (Georgetown, Tex.)2018

TLR-4/microRNA-125a/NF-κB signaling modulates the immune response to Mycobacterium tuberculosis infection.

Wenyi Niu, Bing Sun, Mingying Li, Junwei Cui, Jian Huang, Ligong Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Macrophage states and polarization duringFrontiers in cellular and infection microbiology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Methylprednisolone PromotesMicroorganisms · 2023
    Article
  14. Review
  15. [TRAF6 promotesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Virulence · 2021
    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

6 authors at 1 institution in 1 country.

Wenyi Niua Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
Bing Suna Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
Mingying Lia Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
Junwei Cuia Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
Jian Huanga Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
Ligong Zhanga Department of Tuberculosis , The First Affliated Hospital of Xinxiang Medical University , Weihui , China.
First Affiliated Hospital of Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis (TB), caused by Mycobacterium tuberculosis, could lead to kinds of clinical disorders and remains a leading global health problem, resulting in great morbidity and mortality worldwide. Previous studies have firmly demonstrated that M. tuberculosis (M.tb) has evolved to utilize different mechanisms to evade or attenuate the host immune response, such as regulation of immune-related genes by modulation of miRNAs of host or bacteria. However, the knowledge of functions of miRNAs during M.tb infection remains limited. Here, we reported that a host microRNA, miR-125a, was significantly up-regulated by M.tb infection in both RAW264.7 and THP-1cells, in a TLR4 signaling-dependent manner. Subsequently, our results demonstrated that miR-125a was a negative regulator of NF-kB pathway by directly targeting TRAF6, resulting in the suppression of cytokines, attenuation of immune response and promotion of M.tb survival. Taken together, our findings provide a novel detailed molecular mechanism in which miR-125a was enhanced to inhibit inflammatory cytokines secretion and attenuate the immune response during M.tb infection in RAW264.7 and THP-1 cells, and suggest an intrinsic a promising anti-M.tb therapeutic target.

Indexed as

Signal TransductionAnimalsCell LineCytokinesHumansInflammationIntracellular Signaling Peptides and ProteinsMacrophagesMiceMicroRNAsNF-kappa BRAW 264.7 CellsTNF Receptor-Associated Factor 6Toll-Like Receptor 4TranscriptomeTuberculosis, PulmonaryCytokinesIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN125 microRNA, humanNF-kappa BTifab protein, humanTLR4 protein, humanTNF Receptor-Associated Factor 6Toll-Like Receptor 4miR-125aMycobacterium tuberculosisNF-kBTLR-4TRAF6

Identifiers

PMID30153074
PMCPMC6152532
OpenAlexW2889303412

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.