Abstract
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, presents a variable clinical course, varying from asymptomatic to serious debilitating pathologies with cardiac, digestive or cardio-digestive impairment. Previous studies using two clonal T. cruzi populations, Col1.7G2 (T. cruzi I) and JG (T. cruzi II) demonstrated that there was a differential tissue distribution of these parasites during infection in BALB/c mice, with predominance of JG in the heart. To date little is known about the mechanisms that determine this tissue selection. Upon infection, host cells respond producing several factors, such as reactive oxygen species (ROS), cytokines, among others. Herein and in agreement with previous data from the literature we show that JG presents a higher intracellular multiplication rate when compared to Col1.7G2. We also showed that upon infection cardiomyocytes in culture may increase the production of oxidative species and its levels are higher in cultures infected with JG, which expresses lower levels of antioxidant enzymes. Interestingly, inhibition of oxidative stress severely interferes with the intracellular multiplication rate of JG. Additionally, upon H2O2-treatment increase in intracellular Ca2+ and oxidants were observed only in JG epimastigotes. Data presented herein suggests that JG and Col1.7G2 may sense extracellular oxidants in a distinct manner, which would then interfere differently with their intracellular development in cardiomyocytes.
Highlights
Chagas disease, caused by the protozoan Trypanosoma cruzi, is an important health problem affecting about 6 to 7 million people worldwide [1]
It has been suggested that parasite differential tissue tropism is responsible for the development of the distinct clinical forms
Upon infection, cardiomyocytes increase the production of oxidative species, especially in cultures infected with JG and inhibition of oxidative stress severely interfered with the intracellular multiplication rate of JG
Summary
Chagas disease, caused by the protozoan Trypanosoma cruzi, is an important health problem affecting about 6 to 7 million people worldwide [1]. Previous studies conducted by our group showed that distinct parasite populations are found in different organs of infected patients [7], reinforcing data on the existence of a differential tissue tropism, probably related to the development of the diverse clinical forms [8,9,10]. Later, we studied this tissue tropism by performing mixed infections in BALB/c mice with two clonal populations of T. cruzi, Col1.7G2 (T. cruzi I) and JG (T. cruzi II), and detection of parasites directly from infected tissues. The mechanisms that define this selection are still poorly understood
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