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MEM INST OSWALDO CRUZ, RIO DE JANEIRO, Vol. 113 | 2018
PAGES: DOI: 10.1590/0074-02760170332 Full paper
Complement system contributes to modulate the infectivity of susceptible TcI strains of Trypanosoma cruzi

Ruben D Arroyo-Olarte1, Ignacio Martínez1, Mayra Cruz-Rivera2, Fela Mendlovic2,3, Bertha Espinoza1,+

1Universidad Nacional Autónoma de México, Instituto de Investigaciones Biomedicas, Departamento de Immunología, Ciudad de Mexico, Mexico
2Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Microbiología y Parasitología, Ciudad de Mexico, Mexico
3Universidad Anahuac, Facultad de Ciencias de la Salud, Mexico Norte, Estado de Mexico, Mexico

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Abstract

BACKGROUND Trypanosoma cruzi is a protozoan parasite and an etiological agent of Chagas disease. There is a wide variability in the clinical outcome of its infection, ranging from asymptomatic individuals to those with chronic fatal mega syndromes. Both parasite and host factors, as well as their interplay, are thought to be involved in the process.

OBJECTIVES To evaluate the resistance to complement-mediated killing in two T. cruzi TcI strains with differential virulence and the subsequent effect on their infectivity in mammalian cells.

METHODS Tissue-culture derived trypomastigotes of both strains were incubated in guinea pig serum and subjected to flow cytometry in order to determine their viability and complement activations. Trypomastigotes were also incubated on host cells monolayers in the presence of serum, and infectivity was evaluated under different conditions of complement pathway inhibition. Relative expression of the main parasite-specific complement receptors between the two strains was assessed by quantitative real-time polymerase chain reaction.

FINDINGS In this work, we showed that two TcI strains, one with lower virulence (Ninoa) compared to the other (Qro), differ in their resistance to the lytic activity of complement system, hence causing a compromised ability of Ninoa strain to invade mammalian cells. These results correlate with the three-fold lower messenger RNA (mRNA) levels of complement regulatory protein (CRP), trypomastigote-decay acceleration factor (T-DAF), and complement C2 receptor inhibitor trispanning (CRIT) in Ninoa compared to those in Qro. On the other hand, calreticulin (CRT) mRNA and surface protein levels were higher in Ninoa strain and promoted its infectivity when the lectin pathway of the complement system was inhibited.

MAIN CONCLUSIONS This work suggests the complex interplay of CRP, T-DAF, CRIT, and CRT, and the diagnostic value of mRNA levels in the assessment of virulence potential of T. cruzi strains, particularly when dealing with isolates with similar genetic background.

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Financial support: Program UNAM-DGAPA-PAPIIT, IN208417 and UNAM-DGAPA post-doctoral fellowship.
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Received 15 August 2017
Accepted 28 December 2017