Evidence map›Paper›PMID 15085199›Full record

ArticleThe Journal of clinical investigation2004

The endogenous cannabinoid system protects against colonic inflammation.

Federico Massa, Giovanni Marsicano, Heike Hermann, Astrid Cannich, Krisztina Monory, Benjamin F Cravatt, Gian-Luca Ferri, Andrei Sibaev, Martin Storr, Beat Lutz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 3 pooled it
24.9field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 3 syntheses or guidelines pooled it, 413 citations in OpenAlex.

  1. Pooled it
  2. Cannabis for the treatment of Crohn's disease.The Cochrane database of systematic reviews · 2018
    Pooled it
  3. Cannabis for the treatment of ulcerative colitis.The Cochrane database of systematic reviews · 2018
    Pooled it
  4. Trial
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  7. Review
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  15. Article
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  18. Article
  19. Cannabinoids and the Gastrointestinal Tract.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2023
    Review
  20. The effect ofJournal of diabetes and metabolic disorders · 2023
    Article

137 more citing papers are in PubMed but not listed here.

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

10 authors at 5 institutions in 3 countries.

Federico MassaGroup Molecular Genetics of Behaviour, Max Planck Institute of Psychiatry, Munich, Germany.
Giovanni Marsicano
Heike Hermann
Astrid Cannich
Krisztina Monory
Benjamin F Cravatt
Gian-Luca Ferri
Andrei Sibaev
Martin Storr
Beat Lutz
Max Planck Institute for Molecular Genetics · DEKlinikum Vest · DEMax Planck Society · DEScripps Research Institute · USUniversity of Cagliari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive inflammatory responses can emerge as a potential danger for organisms' health. Physiological balance between pro- and anti-inflammatory processes constitutes an important feature of responses against harmful events. Here, we show that cannabinoid receptors type 1 (CB1) mediate intrinsic protective signals that counteract proinflammatory responses. Both intrarectal infusion of 2,4-dinitrobenzene sulfonic acid (DNBS) and oral administration of dextrane sulfate sodium induced stronger inflammation in CB1-deficient mice (CB1(-/-)) than in wild-type littermates (CB1(+/+)). Treatment of wild-type mice with the specific CB1 antagonist N-(piperidino-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-pyrazole-3-carboxamide (SR141716A) mimicked the phenotype of CB1(-/-) mice, showing an acute requirement of CB1 receptors for protection from inflammation. Consistently, treatment with the cannabinoid receptor agonist R(-)-7-hydroxy-Delta(6)-tetra-hydrocannabinol-dimethylheptyl (HU210) or genetic ablation of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) resulted in protection against DNBS-induced colitis. Electrophysiological recordings from circular smooth muscle cells, performed 8 hours after DNBS treatment, revealed spontaneous oscillatory action potentials in CB1(-/-) but not in CB1(+/+) colons, indicating an early CB1-mediated control of inflammation-induced irritation of smooth muscle cells. DNBS treatment increased the percentage of myenteric neurons expressing CB1 receptors, suggesting an enhancement of cannabinoid signaling during colitis. Our results indicate that the endogenous cannabinoid system represents a promising therapeutic target for the treatment of intestinal disease conditions characterized by excessive inflammatory responses.

Indexed as

AmidohydrolasesAnimalsColitisDinitrofluorobenzeneDronabinolFatty Acid Amide HydrolasesFemaleGene Expression RegulationMiceMice, Inbred C57BLPiperidinesPyrazolesReceptor, Cannabinoid, CB1RimonabantRNA, Messenger2,4-dinitrofluorobenzene sulfonic acidAmidohydrolasesDinitrofluorobenzeneDronabinolFatty Acid Amide HydrolasesHU 211PiperidinesPyrazolesReceptor, Cannabinoid, CB1RimonabantRNA, Messenger

Identifiers

PMID15085199
PMCPMC385396
OpenAlexW2131051512

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.