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Artículo

IL-6 promotes M2 macrophage polarization by modulating purinergic signaling and regulates the lethal release of nitric oxide during Trypanosoma cruzi infection

Sanmarco, Liliana MariaIcon ; Ponce, Nicolás EricIcon ; Visconti, Laura M.; Eberhardt, NataliaIcon ; Theumer, Martín GustavoIcon ; Minguez, Ángel R.; Aoki, Maria del PilarIcon
Fecha de publicación: 01/2017
Editorial: Elsevier Science
Revista: Biochimica et Biophysica Acta - Molecular Basis of Disease
ISSN: 0925-4439
e-ISSN: 0006-3002
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Inmunología

Resumen

The production of nitric oxide (NO) is a key defense mechanism against intracellular pathogens but it must be tightly controlled in order to avoid excessive detrimental oxidative stress. In this study we described a novel mechanism through which interleukin (IL)-6 mediates the regulation of NO release induced in response to Trypanosoma cruzi infection. Using a murine model of Chagas disease, we found that, in contrast to C57BL/6 wild type (WT) mice, IL-6-deficient (IL6KO) mice exhibited a dramatic increase in plasma NO levels concomitant with a significantly higher amount of circulating IL-1β and inflammatory monocytes. Studies on mouse macrophages and human monocytes, revealed that IL-6 decreased LPS-induced NO production but this effect was abrogated in the presence of anti-IL-1β and in macrophages deficient in the NLRP3 inflammasome. In accordance, while infected WT myocardium exhibited an early shift from microbicidal/M1 to anti-inflammatory/M2 macrophage phenotype, IL6KO cardiac tissue never displayed a dominant M2 macrophage profile that correlated with decreased expression of ATP metabolic machinery and a lower cardiac parasite burden. The deleterious effects of high NO production-induced oxidative stress were evidenced by enhanced cardiac malondialdehyde levels, myocardial cell death and mortality. The survival rate was improved by the treatment of IL-6-deficient mice with a NO production-specific inhibitor. Our data revealed that IL-6 regulates the excessive release of NO through IL-1β inhibition and determines the establishment of an M2 macrophage profile within infected heart tissue.
Palabras clave: Human Monocytes , Il-6 , Trypanosoma Cruzi , Nitric Oxide , Cd39 , Cd73
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/66173
URL: https://www.ncbi.nlm.nih.gov/pubmed/28087471
DOI: http://dx.doi.org/10.1016/j.bbadis.2017.01.006
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Articulos(CIBICI)
Articulos de CENTRO DE INV.EN BIOQUI.CLINICA E INMUNOLOGIA
Citación
Sanmarco, Liliana Maria; Ponce, Nicolás Eric; Visconti, Laura M.; Eberhardt, Natalia; Theumer, Martín Gustavo; et al.; IL-6 promotes M2 macrophage polarization by modulating purinergic signaling and regulates the lethal release of nitric oxide during Trypanosoma cruzi infection; Elsevier Science; Biochimica et Biophysica Acta - Molecular Basis of Disease; 1836; 4; 1-2017; 857-869
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