Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a Murine model of early chronic Chagas disease

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dc.contributor.authorCarrillo, Ileana
dc.contributor.authorRabelo, Rayane Aparecida Nonato
dc.contributor.authorBarbosa, César
dc.contributor.authorRates, Mariana
dc.contributor.authorFuentes-Retamal, Sebastián
dc.contributor.authorGonzález-Herrera, Fabiola
dc.contributor.authorGuzmán-Rivera, Daniela
dc.contributor.authorQuintero, Helena
dc.contributor.authorKemmerling, Ulrike
dc.contributor.authorCastillo, Christian
dc.contributor.authorMachado, Fabiana S.
dc.contributor.authorDíaz-Araya, Guillermo
dc.contributor.authorMaya, Juan D.
dc.date.accessioned2025-03-18T16:43:28Z
dc.date.available2025-03-18T16:43:28Z
dc.date.issued2021-11
dc.descriptionIndexación: Scopus.
dc.description.abstractBackground Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America and is widely distributed worldwide because of migration. In 30% of cases, after years of infection and in the absence of treatment, the disease progresses from an acute asymptomatic phase to a chronic inflammatory cardiomyopathy, leading to heart failure and death. An inadequate balance in the inflammatory response is involved in the progression of chronic Chagas cardiomyopathy. Current therapeutic strategies cannot prevent or reverse the heart damage caused by the parasite. Aspirin-triggered resolvin D1 (AT-RvD1) is a pro-resolving mediator of inflammation that acts through N-formyl peptide receptor 2 (FPR2). AT-RvD1 participates in the modification of cytokine production, inhibition of leukocyte recruitment and efferocytosis, macrophage switching to a nonphlogistic phenotype, and the promotion of healing, thus restoring organ function. In the present study, AT-RvD1 is proposed as a potential therapeutic agent to regulate the pro-inflammatory state during the early chronic phase of Chagas disease. Methodology/Principal findings C57BL/6 wild-type and FPR2 knock-out mice chronically infected with T. cruzi were treated for 20 days with 5 μg/kg/day AT-RvD1, 30 mg/kg/day benznidazole, or the combination of 5 μg/kg/day AT-RvD1 and 5 mg/kg/day benznidazole. At the end of treatment, changes in immune response, cardiac tissue damage, and parasite load were evaluated. The administration of AT-RvD1 in the early chronic phase of T. cruzi infection regulated the inflammatory response both at the systemic level and in the cardiac tissue, and it reduced cellular infiltrates, cardiomyocyte hypertrophy, fibrosis, and the parasite load in the heart tissue. © 2021 Carrillo et al.
dc.description.urihttps://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0009978
dc.identifier.citationPLoS Neglected Tropical Diseases, Volume 15, Issue 11, November 2021, Article number e0009978
dc.identifier.doi10.1371/journal.pntd.0009978
dc.identifier.issn1935-2727
dc.identifier.urihttps://repositorio.unab.cl/handle/ria/63812
dc.language.isoen
dc.publisherPublic Library of Science
dc.rights.licenseAtribución/Reconocimiento 4.0 Internacional CC BY 4.0 Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.es
dc.subjectAnimals
dc.subjectChagas Cardiomyopathy
dc.subjectChronic Disease
dc.subjectDisease Models, Animal
dc.subjectDocosahexaenoic Acids
dc.subjectFemale
dc.subjectHeart
dc.subjectHumans
dc.subjectMale
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMyocardium
dc.subjectNitroimidazoles
dc.subjectParasite Load
dc.subjectReceptors, Formyl Peptide
dc.subjectTrypanosoma cruzi
dc.titleAspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a Murine model of early chronic Chagas disease
dc.typeArtículo
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