Evidence map›Paper›PMID 25942007›Full record

ArticlePloS one2015

mTORC1 Regulates Flagellin-Induced Inflammatory Response in Macrophages.

Wenlei Bao, Yanfeng Wang, Yuting Fu, Xiaoyang Jia, Jiaxin Li, Nyamtsengel Vangan, Lili Bao, Huifang Hao, Zhigang Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 56 citations in OpenAlex.

  1. Observational
  2. Review
  3. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
  4. International journal of molecular sciences · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Flagellin FromFrontiers in immunology · 2021
    Article
  15. Inhibition of the mTORC1/NF-BioMed research international · 2021
    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

9 authors at 1 institution in 1 country.

Wenlei BaoCollege of Life Science, Inner Mongolia University, Hohhot, China.
Yanfeng WangCollege of Life Science, Inner Mongolia University, Hohhot, China.
Yuting FuCollege of Life Science, Inner Mongolia University, Hohhot, China.
Xiaoyang JiaCollege of Life Science, Inner Mongolia University, Hohhot, China.
Jiaxin LiCollege of Life Science, Inner Mongolia University, Hohhot, China.
Nyamtsengel VanganCollege of Life Science, Inner Mongolia University, Hohhot, China.
Lili BaoCollege of Life Science, Inner Mongolia University, Hohhot, China; College of Basic Medical Science, Inner Mongolia Medical University, Hohhot, China.
Huifang HaoCollege of Life Science, Inner Mongolia University, Hohhot, China.
Zhigang WangCollege of Life Science, Inner Mongolia University, Hohhot, China.
Inner Mongolia University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial flagellin triggers inflammatory responses. Phosphoinositide 3-kinase (PI3K) and mammalian target of rapamycin (mTOR) regulate the production of pro- and anti-inflammatory cytokines that are induced by extrinsic antigens, but the function of mTORC1 in flagellin-induced inflammatory response is unknown. The purpose of this study was to examine the role and the mechanism of PI3K/Akt/mTOR pathway in flagellin-induced cytokine expression in mouse macrophages. We observed that flagellin upregulated TNF-α time- and dose-dependently. Flagellin stimulated rapid (<15 min) PI3K/Akt/mTOR phosphorylation that was mediated by TLR5. Inhibition of PI3K with LY294002 and wortmannin, and of mTORC1 with rapamycin decreased flagellin-induced TNF-α and IL-6 expression and cell proliferation. The activation of NF-κB p65 and STAT3 was regulated by mTORC1 via degradation of IκBα and phosphorylation of STAT3 in response to flagellin, respectively. Thus, the PI3K/Akt/mTORC1 pathway regulates the innate immune response to bacterial flagellin. Rapamycin is potential therapy that can regulate host defense against pathogenic infections.

Indexed as

AnimalsCell LineCell ProliferationCell SurvivalChromonesCytokinesDose-Response Relationship, DrugFlagellinGene Expression RegulationInflammationMacrophagesMacrophages, PeritonealMAP Kinase Signaling SystemMechanistic Target of Rapamycin Complex 1MiceMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesCytokinesFlagellinMechanistic Target of Rapamycin Complex 1MorpholinesMultiprotein ComplexesNF-kappa BPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktSTAT3 Transcription FactorToll-Like Receptor 5TOR Serine-Threonine KinasesTumor Necrosis Factor-alpha

Identifiers

PMID25942007
PMCPMC4420466
OpenAlexW1618426011

What OpenQuestion holds

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LicenceCC BY
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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.