Evidence map›Paper›PMID 36127495›Full record

ArticleScientific reports2022

Valproic acid restricts mast cell activation by Listeria monocytogenes.

Rodolfo Soria-Castro, Yatsiri G Meneses-Preza, Gloria M Rodríguez-López, Alfredo Ibarra-Sánchez, Claudia González-Espinosa, Sonia M Pérez-Tapia, Fabián Flores-Borja, Sergio Estrada-Parra, Alma D Chávez-Blanco, Rommel Chacón-Salinas

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

10 authors at 5 institutions in 2 countries.

Rodolfo Soria-CastroDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Carpio Y Plan de Ayala S/N Col. Santo Tomás, C.P. 11340, Mexico City, Mexico.
Yatsiri G Meneses-PrezaDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Carpio Y Plan de Ayala S/N Col. Santo Tomás, C.P. 11340, Mexico City, Mexico.
Gloria M Rodríguez-LópezDepartamento de Microbiología e Inmunología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Alfredo Ibarra-SánchezDepartamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados (Cinvestav), Unidad Sede Sur, Mexico City, Mexico.
Claudia González-EspinosaDepartamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados (Cinvestav), Unidad Sede Sur, Mexico City, Mexico.
Sonia M Pérez-TapiaDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Carpio Y Plan de Ayala S/N Col. Santo Tomás, C.P. 11340, Mexico City, Mexico.
Fabián Flores-BorjaCentre for Oral Immunobiology and Regenerative Medicine, Barts & The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Sergio Estrada-ParraDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Carpio Y Plan de Ayala S/N Col. Santo Tomás, C.P. 11340, Mexico City, Mexico.
Alma D Chávez-BlancoSubdirección de Investigación Básica, Instituto Nacional de Cancerología (INCan), Av. San Fernando No. 22. Col. Sección XVI, C.P. 14080, México City, México. celular_alma@hotmail.com.
Rommel Chacón-SalinasDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional (ENCB-IPN), Carpio Y Plan de Ayala S/N Col. Santo Tomás, C.P. 11340, Mexico City, Mexico. rommelchacons@yahoo.com.mx.
Instituto Politécnico Nacional · MXCenter for Research and Advanced Studies of the National Polytechnic Institute · MXInstituto Nacional de Cancerología · MXQueen Mary University of London · GBUniversidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mast cells (MC) play a central role in the early containment of bacterial infections, such as that caused by Listeria monocytogenes (L.m). The mechanisms of MC activation induced by L.m infection are well known, so it is possible to evaluate whether they are susceptible to targeting and modulation by different drugs. Recent evidence indicates that valproic acid (VPA) inhibits the immune response which favors L.m pathogenesis in vivo. Herein, we examined the immunomodulatory effect of VPA on L.m-mediated MC activation. To this end, bone marrow-derived mast cells (BMMC) were pre-incubated with VPA and then stimulated with L.m. We found that VPA reduced MC degranulation and cytokine release induced by L.m. MC activation during L.m infection relies on Toll-Like Receptor 2 (TLR2) engagement, however VPA treatment did not affect MC TLR2 cell surface expression. Moreover, VPA was able to decrease MC activation by the classic TLR2 ligands, peptidoglycan and lipopeptide Pam3CSK4. VPA also reduced cytokine production in response to Listeriolysin O (LLO), which activates MC by a TLR2-independent mechanism. In addition, VPA decreased the activation of critical events on MC signaling cascades, such as the increase on intracellular Ca

Indexed as

Listeria monocytogenesListeriosisCytokinesHumansLipopeptidesMast CellsNF-kappa BPeptidoglycanToll-Like Receptor 2Valproic AcidCytokinesLipopeptidesNF-kappa BPeptidoglycanToll-Like Receptor 2Valproic Acid

Identifiers

PMID36127495
PMCPMC9489790
OpenAlexW4296774357

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.