Evidence map›Paper›PMID 24358114›Full record

ArticlePloS one2013

MicroRNA-146a represses mycobacteria-induced inflammatory response and facilitates bacterial replication via targeting IRAK-1 and TRAF-6.

Shuo Li, Yan Yue, Wei Xu, Sidong Xiong

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.7field-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

55 citing papers in PubMed, 110 citations in OpenAlex.

  1. Observational
  2. Diagnostic value and prognostic effect of has-miR-151a-3p in tuberculosis.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026
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  6. Journal of clinical tuberculosis and other mycobacterial diseases · 2024
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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 2 institutions in 1 country.

Shuo LiInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.
Yan YueJiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
Wei XuJiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
Sidong XiongInstitute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China ; Jiangsu Provincial Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.
Shanghai Medical College of Fudan University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApart from triggering host immune responses, macrophages also act as a major reservoir for mycobacteria. For better survival, mycobacteria have evolved various mechanisms to modulate the production of proinflammatory cytokines in macrophages, and manipulation of micro-RNA (miRNA) expression has been considered as an important one. METHODOLOGY/PRINCIPAL

findingsIn this study, we found that miR-146a expression was significantly increased in a time- and dose-dependent manner in mycobacteria-infected macrophages. It could obviously reduce the induction of proinflammatory cytokines TNF-α, IL-1β, IL-6 and chemokine MCP-1 by targeting interleukin-1 receptor-associated kinase-1 (IRAK-1) and TNF receptor-associated factor-6 (TRAF-6), two key elements involved in the TLR/NF-κB signaling pathway cascades. Consistent with the anti-inflammation effect, a higher bacterial burden was seen in miR-146a mimics-treated macrophages. CONCLUSION/SIGNIFICANCE: Here, we demonstrated that mycobacteria-induced miR-146a could modulate inflammatory response by targeting IRAK1 and TRAF6 and facilitate mycobacteria replication in macrophages.

Indexed as

MycobacteriumAnimalsInflammationInterleukin-1 Receptor-Associated KinasesMacrophagesMiceMice, Inbred C57BLMicroRNAsSignal TransductionTNF Receptor-Associated Factor 6Interleukin-1 Receptor-Associated KinasesMicroRNAsMirn146 microRNA, mouseTNF Receptor-Associated Factor 6

Identifiers

PMID24358114
PMCPMC3864784
OpenAlexW2152451121

What OpenQuestion holds

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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.