Evidence map›Paper›PMID 34057753›Full record

ArticleJournal of leukocyte biology2021

Severe COVID-19 is marked by dysregulated serum levels of carboxypeptidase A3 and serotonin.

Rodolfo Soria-Castro, Yatsiri G Meneses-Preza, Gloria M Rodríguez-López, Sandra Romero-Ramírez, Víctor A Sosa-Hernández, Rodrigo Cervantes-Díaz, Alfredo Pérez-Fragoso, José J Torres-Ruíz, Diana Gómez-Martín, Marcia Campillo-Navarro and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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  4. International journal of molecular sciences · 2024
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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

16 authors at 5 institutions in 1 country.

Rodolfo Soria-CastroDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Yatsiri G Meneses-PrezaDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Gloria M Rodríguez-LópezDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Sandra Romero-RamírezRed de Apoyo a la Investigación, Universidad Nacional Autónoma de México e Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Víctor A Sosa-HernándezRed de Apoyo a la Investigación, Universidad Nacional Autónoma de México e Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Rodrigo Cervantes-DíazRed de Apoyo a la Investigación, Universidad Nacional Autónoma de México e Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Alfredo Pérez-FragosoDepartamento de Inmunología y Reumatología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
José J Torres-RuízDepartamento de Atención Institucional Continua y Urgencias, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Diana Gómez-MartínDepartamento de Inmunología y Reumatología, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Marcia Campillo-NavarroResearch Coordination, Centro Médico Nacional 20 de Noviembre, ISSSTE, Mexico City, Mexico.
Violeta D Álvarez-JiménezLab. de Biología Molecular y Bioseguridad Nivel 3. Centro Médico Naval-SEMAR, Mexico City, Mexico.
Sonia M Pérez-TapiaDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Alma D Chávez-BlancoDivisión de Ciencia Básica, Instituto Nacional de Cancerología (INCan), Mexico City, Mexico.
Sergio Estrada-ParraDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
José L Maravillas-MonteroRed de Apoyo a la Investigación, Universidad Nacional Autónoma de México e Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Rommel Chacón-SalinasDepartamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, ENCB-IPN, Mexico City, Mexico.
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXInstituto Politécnico Nacional · MXCenter for Research and Advanced Studies of the National Polytechnic Institute · MXInstitute for Social Security and Services for State Workers · MXInstituto Nacional de Cancerología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune response plays a critical role in the pathophysiology of SARS-CoV-2 infection ranging from protection to tissue damage and all occur in the development of acute respiratory distress syndrome (ARDS). ARDS patients display elevated levels of inflammatory cytokines and innate immune cells, and T and B cell lymphocytes have been implicated in this dysregulated immune response. Mast cells are abundant resident cells of the respiratory tract and are able to release different inflammatory mediators rapidly following stimulation. Recently, mast cells have been associated with tissue damage during viral infections, but their role in SARS-CoV-2 infection remains unclear. In this study, we examined the profile of mast cell activation markers in the serum of COVID-19 patients. We noticed that SARS-CoV-2-infected patients showed increased carboxypeptidase A3 (CPA3) and decreased serotonin levels in their serum when compared with symptomatic SARS-CoV-2-negative patients. CPA3 levels correlated with C-reactive protein, the number of circulating neutrophils, and quick SOFA. CPA3 in serum was a good biomarker for identifying severe COVID-19 patients, whereas serotonin was a good predictor of SARS-CoV-2 infection. In summary, our results show that serum CPA3 and serotonin levels are relevant biomarkers during SARS-CoV-2 infection. This suggests that mast cells and basophils are relevant players in the inflammatory response in COVID-19 and may represent targets for therapeutic intervention.

Indexed as

BiomarkersCarboxypeptidases ACOVID-19HumansInflammationInflammation MediatorsMast CellsSARS-CoV-2SerotoninSeverity of Illness IndexBiomarkersCarboxypeptidases ACPA3 protein, humanInflammation MediatorsSerotonincarboxypeptidase A3COVID-19Mast cellSARS-CoV-2serotonin

Identifiers

PMID34057753
PMCPMC8242632
OpenAlexW3128796809

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.