Evidence map›Paper›PMID 33807975›Full record

ArticlePharmaceuticals (Basel, Switzerland)2021

Cannabidiol (CBD) Alters the Functionality of Neutrophils (PMN). Implications in the Refractory Epilepsy Treatment.

Claudia Taborda Gómez, Fabiana Lairion, Marisa Repetto, Miren Ettcheto, Amalia Merelli, Alberto Lazarowski, Jerónimo Auzmendi

Open access · goldAbstract read
In one paragraph

Article in Pharmaceuticals (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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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

7 authors at 3 institutions in 2 countries.

Claudia Taborda GómezDepartamento de Bioquímica Clínica, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires C1120AAF, Argentina.
Fabiana LairionDepartamento de Química Analítica y Fisicoquímica, Facultad de Farmacia y Bioquímica, Instituto de Bioquímica y Medicina Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad de Buenos Aires, (IBIMOL, UBA-CONICET), Buenos Aires C1113AAD, Argentina.
Marisa RepettoDepartamento de Química Analítica y Fisicoquímica, Facultad de Farmacia y Bioquímica, Instituto de Bioquímica y Medicina Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad de Buenos Aires, (IBIMOL, UBA-CONICET), Buenos Aires C1113AAD, Argentina.
Miren EttchetoDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Science, Institute of Neuroscience, University of Barcelona, 08193 Barcelona, Spain.ORCID 0000-0002-4301-7297
Amalia MerelliDepartamento de Bioquímica Clínica, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires C1120AAF, Argentina.
Alberto LazarowskiDepartamento de Bioquímica Clínica, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires C1120AAF, Argentina.ORCID 0000-0001-8979-7631
Jerónimo AuzmendiDepartamento de Bioquímica Clínica, Facultad de Farmacia y Bioquímica, Instituto de Fisiopatología y Bioquímica Clínica (INFIBIOC), Universidad de Buenos Aires, Buenos Aires C1120AAF, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad de Buenos Aires · ARBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

UBACyT 20720170200024BA
6 · The paper itself

Abstract

Cannabidiol (CBD), a lipophilic cannabinoid compound without psychoactive effects, has emerged as adjuvant of anti-epileptic drugs (AEDs) in the treatment of refractory epilepsy (RE), decreasing the severity and/or frequency of seizures. CBD is considered a multitarget drug that could act throughout the canonical endocannabinoid receptors (CB1-CB2) or multiple non-canonical pathways. Despite the fact that the CBD mechanism in RE is still unknown, experiments carried out in our laboratory showed that CBD has an inhibitory role on P-glycoprotein excretory function, highly related to RE. Since CB2 is expressed mainly in the immune cells, we hypothesized that CBD treatment could alter the activity of polymorphonuclear neutrophils (PMNs) in a similar way that it does with microglia/macrophages and others circulating leukocytes. In vitro, CBD induced PMN cytoplasmatic vacuolization and proapoptotic nuclear condensation, associated with a significantly decreased viability in a concentration-dependent manner, while low CBD concentration decreased PMN viability in a time-dependent manner. At a functional level, CBD reduced the chemotaxis and oxygen consumption of PMNs related with superoxide anion production, while the singlet oxygen level was increased suggesting oxidative stress damage. These results are in line with the well-known CBD anti-inflammatory effect and support a potential immunosuppressor role on PMNs that could promote an eventual defenseless state during chronic treatment with CBD in RE.

Indexed as

cannabidiolchemotaxisoxidative stressoxygen consumptionpolymorphonuclear neutrophils (PMNs)refractory epilepsy

Identifiers

PMID33807975
PMCPMC8001508
OpenAlexW3133989845

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.