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dc.contributor.author
Cutrullis, Romina Andrea
dc.contributor.author
Petray, Patricia Beatriz
dc.contributor.author
Corral, Ricardo Santiago
dc.date.available
2018-06-06T14:33:06Z
dc.date.issued
2017-02
dc.identifier.citation
Cutrullis, Romina Andrea; Petray, Patricia Beatriz; Corral, Ricardo Santiago; MIF-driven activation of macrophages induces killing of intracellular Trypanosoma cruzi dependent on endogenous production of tumor necrosis factor, nitric oxide and reactive oxygen species; Elsevier Gmbh; Immunobiology; 222; 2; 2-2017; 423-431
dc.identifier.issn
0171-2985
dc.identifier.uri
http://hdl.handle.net/11336/47457
dc.description.abstract
The proinflammatory cytokine macrophage migration inhibitory factor (MIF) is a key player in innate immunity. MIF has been considered critical for controlling acute infection by the protozoan Trypanosoma cruzi, but the underlying mechanisms are poorly understood. Our study aimed to analyze whether MIF could favor microbicidal activity of the macrophage, a site where T. cruzi grows and the initial effector cell against this parasite. Using murine macrophages infected in vitro, we examined the effect of MIF on their parasiticidal ability and attempted to identify inflammatory agents involved in MIF-induced protection. Our findings show that MIF is readily secreted from peritoneal macrophages upon T. cruzi infection. MIF activates both primary and J774 phagocytes boosting the endogenous production of tumor necrosis factor-alpha via mitogen-activated protein kinase p38 signaling, as well as the release of nitric oxide and reactive oxygen species, leading to enhanced pathogen elimination. MIF can also potentiate the effect of interferon-gamma on T. cruzi killing by J774 and mouse peritoneal macrophages, rendering these cells more competent in reducing intracellular parasite burden. The present results unveil a novel innate immune pathway that contributes to host defense and broaden our understanding of the regulation of inflammatory mediators implicated in early parasite containment that is decisive for resistance to T. cruzi infection.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Gmbh
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Trypanosoma Cruzi Infection
dc.subject
Macrophage Activation
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Parasiticidal Activity
dc.subject
Macrophage Migration Inhibitory Factor
dc.subject
Tumor Necrosis Factor
dc.subject.classification
Salud Ocupacional
dc.subject.classification
Ciencias de la Salud
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
MIF-driven activation of macrophages induces killing of intracellular Trypanosoma cruzi dependent on endogenous production of tumor necrosis factor, nitric oxide and reactive oxygen species
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-06T13:38:03Z
dc.journal.volume
222
dc.journal.number
2
dc.journal.pagination
423-431
dc.journal.pais
Alemania
dc.journal.ciudad
Stuttgary
dc.description.fil
Fil: Cutrullis, Romina Andrea. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños ; Argentina
dc.description.fil
Fil: Petray, Patricia Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones en Microbiología y Parasitología Médica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en Microbiología y Parasitología Médica; Argentina
dc.description.fil
Fil: Corral, Ricardo Santiago. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños ; Argentina
dc.journal.title
Immunobiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1016/j.imbio.2016.08.007
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0171298516303485


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