Trypanosoma cruziMexican Strains Differentially Modulate Surface Markers and Cytokine Production in Bone Marrow-Derived Dendritic Cells from C57BL/6 and BALB/c Mice

Abstract

Dendritic cells (DCs) are a type of antigen-presenting cells that play an important role in the immune response against Trypanosoma cruzi, the causative agent of Chagas disease. In vitro and in vivo studies have shown that the modulation of these cells by this parasite can directly affect the innate and acquired immune response of the host in order to facilitate its biological cycle and the spreading of the species. Many studies show the mechanisms by which T. cruzi modulates DCs, but the interaction of these cells with the Mexican strains of T. cruzi such as Ninoa and INC5 has not yet been properly investigated. Here, we evaluated whether Ninoa and INC5 strains evaded the immunity of their hosts by modulating the biology and function of murine DCs. The CL-Brener strain was used as the reference strain. Herein, it was demonstrated that Ninoa was more infective toward bone marrow-derived dendritic cells (BMDCs) than INC5 and CL-Brener strains in both BMDCs of BALB/c and C57BL/6 mice. Mexican strains of T. cruzi induced different cytokine patterns. In BMDCs obtained from BALB/c mice, Ninoa strain led to the reduction in IL-6 and increased IL-10 production, while in C57BL/6 mice Ninoa strain considerably increased the productions of TNF-α and IL-10. Also, Ninoa and INC5 differentially modulated BMDC expressions of MHC-II, TLR2, and TLR4 in both BALB/c and C57BL/6 mice compared to Brazilian strain CL-Brener. These results indicate that T. cruzi Mexican strains differentially infect and modulate MHC-II, toll-like receptors, and cytokine production in DCs obtained from C57BL/6 and BALB/c mice, suggesting that these strains have developed particular modulatory strategies to disrupt DCs and, consequently, the host immune responses.

Circulating miR-146a as a possible candidate biomarker in the indeterminate phase of Chagas disease

“…Ruíz-Sánchez et al determined in 2005 that some Mexican isolates are predominantly TcI DTU [ 8 ]. Ninoa is a cardiotrophic and myotropic strain and is classified into TcI [ 7 , 9 , 10 ].…”

Characterisation of Macrophage Polarisation in Mice Infected with Ninoa Strain of Trypanosoma cruzi

“…The small differences in blood parasite behaviour and heart damage between C57BL/6 and BALB/c mice could be explained by the fact that different strains of T. cruzi have different infectivity potentials [31]. In this sense, the Tc1 genotype, to which the Ninoa strain belongs, has a high intraspecific genetic and phenotypic diversity [32], which is determinant to recognize the surface molecules of the parasite by immune cells [33]. These characteristics could explain how the Ninoa strain exhibits more modulating behaviours of the immune response compared to other strains of T. cruzi [32].…”

“…In this sense, the Tc1 genotype, to which the Ninoa strain belongs, has a high intraspecific genetic and phenotypic diversity [32], which is determinant to recognize the surface molecules of the parasite by immune cells [33]. These characteristics could explain how the Ninoa strain exhibits more modulating behaviours of the immune response compared to other strains of T. cruzi [32]. Thus, it is possible that the Ninoa strain could manipulate immune cells to produce a tolerogenic cytokines profile regardless of the genetic background of the mouse.…”

Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process

“…Changes in galectin levels were correlated with the progression and worse prognosis of intestinal diseases such as colorectal cancer, colorectal adenoma, rectal cancer, and Crohn's disease [ 180 ]. In CD, galectin-1 (gal-1) and galectin-3 (gal-3) production was analyzed in experimental in vitro cardiac form models and in infected patients with Chagas heart disease in the acute and chronic phases [ 181 ]. Information regarding the profile and function of these proteins in the megacolon is lacking.…”