dc.creatorBomfim, Lays Gisele Santos
dc.creatorMagalhães, Lucas S
dc.creatorSantos Filho, Marcello Augusto Anchieta
dc.creatorPeres, Nalu Teixeira de Aguiar
dc.creatorCorrêa, Cristiane B
dc.creatorTanajura, Diego Moura
dc.creatorSilva, Angela Maraia da
dc.creatorLipscomb, Michael W
dc.creatorBorges, Valéria de Matos
dc.creatorJesus, Amélia Ribeiro de
dc.creatorAlmeida, Roque Pacheco de
dc.creatorMoura, Tatiana Rodrigues de
dc.date2018-02-27T14:05:57Z
dc.date2018-02-27T14:05:57Z
dc.date2017
dc.date.accessioned2023-09-26T23:49:49Z
dc.date.available2023-09-26T23:49:49Z
dc.identifierBOMFIM, L. G. S. et al. Leishmania infantumInduces the Release of sTREM-1 in Visceral Leishmaniasis. Frontiers in Microbiology, v. 8, Article 2265, 2017.
dc.identifier1664-302X
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/24965
dc.identifier10.3389/fmicb.2017.02265
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8894669
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), MCTI/CNPQ/Universal 14/2014—460743/2014-7 (TdM) and PROCAD/CASADINHO—n◦552721/2011-5 (RA); Fundação de Apoio à Pesquisa e à Inovação Tecnológica do Estado de Sergipe FAPITEC/SE/FUNTEC/CNPq n◦12/2009—019.203.02712/2009-8 (AJ); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Programa Nacional de Incentivo à Pesquisa em Parasitologia Básica, Edital No 032/2010 (AJ); National Institute Health, NIH Grant# SC2GM103741 (ML); Department of Defense, DOD Grant# W911NF-14-1-0123, (ML); and National Science Foundation, NSF Grant# 1428768, (ML).
dc.descriptionVisceral leishmaniasis (VL) is a systemic transmissible disease that remains to be a major global health problem. The inflammatory response during VL is characterized by the release of several cytokines and other pro-inflammatory mediators. Triggering Receptor Expressed on Myeloid Cells (TREM) are a group of evolutionarily conserved membrane-bound surface receptors expressed on neutrophils and monocytes. Engagement of TREM-1 directs intracellular signaling events that drive cytokine production, degranulation, and phagocytosis. In certain inflammatory-associated diseases, TREM-1 can also be found as a soluble form (sTREM-1), which can negatively regulate TREM-1 receptor signaling. In these studies, we now find that high levels of circulating sTREM-1 correlate directly with VL disease severity. In particular, high levels of sTREM-1 were observed in non-survivor VL patients. Furthermore, these levels of sTREM-1 positively correlated with liver size and negatively correlated with leukocyte counts and hemoglobin concentration. Moreover, we found that neutrophils exposurein vitrotoLeishmania infantummodulates TREM-1, DAP12, and IL-8 gene expression, while also increasing release of sTREM-1. Finally, results revealed that higher sTREM-1 levels are associated with increasing parasite ratio. Taken together, these studies suggest thatL. infantummay modulate TREM-1 in neutrophils and high levels of this molecule is associated with severe VL.
dc.formatapplication/pdf
dc.languageeng
dc.publisherFrontiers Media
dc.rightsopen access
dc.subjectLeishmaniose visceral
dc.subjectLeishmania infantum
dc.subjectNeutrófilos
dc.subjectsTREM-1
dc.subjectTREM-1
dc.subjectVisceral leishmaniasis
dc.subjectLeishmania infantum
dc.subjectNeutrophils
dc.subjectsTREM-1
dc.subjectTREM-1
dc.titleLeishmania infantumInduces the Release of sTREM-1 in Visceral Leishmaniasis
dc.typeArticle


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