Evidence map›Paper›PMID 24349442›Full record

ArticlePloS one2013

A trifluoromethyl analogue of celecoxib exerts beneficial effects in neuroinflammation.

Alessandra Di Penta, Asako Chiba, Iraide Alloza, Ane Wyssenbach, Takashi Yamamura, Pablo Villoslada, Sachiko Miyake, Koen Vandenbroeck

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Spatial mapping of the AA-PGEActa neuropathologica · 2025
    Article
  5. Article
  6. Article
  7. The role of microglia in multiple sclerosis.Neuropsychiatric disease and treatment · 2017
    Review
  8. Article
  9. Review
  10. Article
  11. 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 5 institutions in 2 countries.

Alessandra Di PentaNeurogenomiks Laboratory, University of Basque Country (UPV/ EHU), Zamudio, Spain ; Achucarro Basque Center for Neuroscience, Zamudio, Spain.
Asako ChibaDepartment of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan ; Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Iraide AllozaNeurogenomiks Laboratory, University of Basque Country (UPV/ EHU), Zamudio, Spain ; Achucarro Basque Center for Neuroscience, Zamudio, Spain ; IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
Ane WyssenbachNeurotek Laboratory, University of Basque Country (UPV/EHU), Zamudio, Spain.
Takashi YamamuraDepartment of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Pablo VillosladaCenter of Neuroimmunology, Institute of Biomedical Research August Pi Sunyer (IDIBAPS) - Hospital Clinic of Barcelona, Barcelona, Spain.
Sachiko MiyakeDepartment of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan ; Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Koen VandenbroeckNeurogenomiks Laboratory, University of Basque Country (UPV/ EHU), Zamudio, Spain ; Achucarro Basque Center for Neuroscience, Zamudio, Spain ; IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
National Center of Neurology and Psychiatry · JPUniversity of the Basque Country · ESAchucarro Basque Center for Neuroscience · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESIkerbasque · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celecoxib is a selective cyclooxygenase-2 (COX2) inhibitor. We have previously shown that celecoxib inhibits experimental autoimmune encephalomyelitis (EAE) in COX-2-deficient mice, suggestive for a mode of action involving COX2-independent pathways. In the present study, we tested the effect of a trifluoromethyl analogue of celecoxib (TFM-C) with 205-fold lower COX-2 inhibitory activity in two models of neuroinflammation, i.e. cerebellar organotypic cultures challenged with LPS and the EAE mouse model for multiple sclerosis. TFM-C inhibited secretion of IL-1β, IL-12 and IL-17, enhanced that of TNF-α and RANTES, reduced neuronal axonal damage and protected from oxidative stress in the organotypic model. TFM-C blocked TNF-α release in microglial cells through a process involving intracellular retention, but induced TNF-α secretion in primary astrocyte cultures. Finally, we demonstrate that TFM-C and celecoxib ameliorated EAE with equal potency. This coincided with reduced secretion of IL-17 and IFN-γ by MOG-reactive T-cells and of IL-23 and inflammatory cytokines by bone marrow-derived dendritic cells. Our study reveals that non-coxib analogues of celecoxib may have translational value in the treatment of neuro-inflammatory conditions.

Indexed as

AnimalsAstrocytesAxonsCelecoxibCells, CulturedCyclooxygenase 2 InhibitorsCytokinesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalInflammationLipopolysaccharidesMiceMultiple SclerosisPyrazolesSulfonamidesCelecoxibCyclooxygenase 2 InhibitorsCytokinesLipopolysaccharidesPyrazolesSulfonamides

Identifiers

PMID24349442
PMCPMC3859644
OpenAlexW2087874555

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.