Evidence map›Paper›PMID 31479429›Full record

Observational studyJCI insight2019

Monocyte glycolysis determines CD8+ T cell functionality in human Chagas disease.

Liliana María Sanmarco, Natalia Eberhardt, Gastón Bergero, Luz Piedad Quebrada Palacio, Pamela Martino Adami, Laura Marina Visconti, Ángel Ramón Minguez, Yolanda Hernández-Vasquez, Eugenio Antonio Carrera Silva, Laura Morelli and 2 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  6. The intersection of hostMicrobiology and molecular biology reviews : MMBR · 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

12 authors at 5 institutions in 2 countries.

Liliana María SanmarcoUniversidad Nacional de Córdoba, Facultad de Ciencias Químicas, Departamento de Bioquímica Clínica, Córdoba, Argentina.
Natalia EberhardtUniversidad Nacional de Córdoba, Facultad de Ciencias Químicas, Departamento de Bioquímica Clínica, Córdoba, Argentina.
Gastón BergeroUniversidad Nacional de Córdoba, Facultad de Ciencias Químicas, Departamento de Bioquímica Clínica, Córdoba, Argentina.
Luz Piedad Quebrada PalacioInstituto Nacional de Parasitología "Dr. Mario Fatala Chabén," Buenos Aires, Argentina.
Pamela Martino AdamiLaboratorio de Amiloidosis y Neurodegeneración, Fundación Instituto Leloir, Buenos Aires, Argentina.
Laura Marina ViscontiHospital Nuestra Señora de la Misericordia, Córdoba, Argentina.
Ángel Ramón MinguezHospital Nuestra Señora de la Misericordia, Córdoba, Argentina.
Yolanda Hernández-VasquezInstituto Nacional de Parasitología "Dr. Mario Fatala Chabén," Buenos Aires, Argentina.
Eugenio Antonio Carrera SilvaLaboratorio de Trombosis Experimental, Instituto de Medicina Experimental, Academia Nacional de Medicina, CONICET, Buenos Aires, Argentina.
Laura MorelliLaboratorio de Amiloidosis y Neurodegeneración, Fundación Instituto Leloir, Buenos Aires, Argentina.
Miriam PostanInstituto Nacional de Parasitología "Dr. Mario Fatala Chabén," Buenos Aires, Argentina.
Maria Pilar AokiUniversidad Nacional de Córdoba, Facultad de Ciencias Químicas, Departamento de Bioquímica Clínica, Córdoba, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARInstitute of Parasitology · CZAcademia Nacional de Medicina · ARServicio Diabetología Hospital Córdoba · ARUniversidad Nacional de Córdoba · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chagas disease is a lifelong pathology resulting from Trypanosoma cruzi infection. It represents one of the most frequent causes of heart failure and sudden death in Latin America. Herein, we provide evidence that aerobic glycolytic pathway activation in monocytes drives nitric oxide (NO) production, triggering tyrosine nitration (TN) on CD8+ T cells and dysfunction in patients with chronic Chagas disease. Monocytes from patients exhibited a higher frequency of hypoxia-inducible factor 1α and increased expression of its target genes/proteins. Nonclassical monocytes are expanded in patients' peripheral blood and represent an important source of NO. Monocytes entail CD8+ T cell surface nitration because both the frequency of nonclassical monocytes and that of NO-producing monocytes positively correlated with the percentage of TN+ lymphocytes. Inhibition of glycolysis in in vitro-infected peripheral blood mononuclear cells decreased the inflammatory properties of monocytes/macrophages, diminishing the frequency of IL-1β- and NO-producing cells. In agreement, glycolysis inhibition reduced the percentage of TN+CD8+ T cells, improving their functionality. Altogether, these results clearly show that glycolysis governs oxidative stress on monocytes and modulates monocyte-T cell interplay in human chronic Chagas disease. Understanding the pathological immune mechanisms that sustain an inflammatory environment in human pathology is key to designing improved therapies.

Indexed as

AdultAnimalsCase-Control StudiesCD8-Positive T-LymphocytesCell CommunicationChagas DiseaseChlorocebus aethiopsCoculture TechniquesFemaleGlycolysisHumansLymphocyte ActivationMaleMiddle AgedMonocytesNitric OxideNitric OxideProtozoan ProteinsTyrosineCardiovascular diseaseGlucose metabolismImmunologyMetabolismMonocytes

Identifiers

PMID31479429
PMCPMC6795286
OpenAlexW2971998570

What Socratic 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 Socratic graph.