Leishmania infantum induces the release of sTREM-1 in visceral leishmaniasis

Lays G.S. Bomfim, Lucas S. Magalhães, Marcello A.A. Santos-Filho, Nalu T.A. Peres, Cristiane B. Corrêa, Diego M. Tanajura, Angela M. Silva, Michael W. Lipscomb, Valéria M. Borges, Amélia R. Jesus, Roque P. Almeida, Tatiana R. de Moura

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12 Scopus citations


Visceral 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 exposure in vitro to Leishmania infantum modulates 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 that L. infantum may modulate TREM-1 in neutrophils and high levels of this molecule is associated with severe VL.

Original languageEnglish (US)
Article number2265
JournalFrontiers in Microbiology
Issue numberNOV
StatePublished - Nov 16 2017
Externally publishedYes

Bibliographical note

Funding Information:
We thank to the Pediatric and Infectious Disease Clinic Group from the University Hospital, Universidade Federal de Sergipe. This work was supported by grants: Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), MCTI/CNPQ/Universal 14/2014-460743/2014-7 (TdM) and PROCAD/CASADINHO-no 552721/2011-5 (RA); Fundação de Apoio à Pesquisa e à Inovação Tecnológica do Estado de Sergipe FAPITEC/SE/FUNTEC/CNPq no 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).

Publisher Copyright:
© 2017 Bomfim, Magalhães, Santos-Filho, Peres, Corrêa, Tanajura, Silva, Lipscomb, Borges, Jesus, Almeida and de Moura.


  • Leishmania infantum
  • Neutrophils
  • STREM-1
  • TREM-1
  • Visceral leishmaniasis


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