Abstract
A murine model was used to study the histopathological aspects and cytokine expression levels in skeletal muscle provoked by the infection with Mexican TcI strains. BALB/c mice were inoculated with the virulent Querétaro strain and the nonvirulent Ninoa strain. Parasite numbers were counted in blood and skeletal muscle at different times post-infection, and real time-PCR expression levels of the cytokines IL-12, IL-4, IL-10, IFN-γ, and TNF-α were evaluated. In the acute phase of infection, a high parasitic load, both in blood and skeletal muscle, was detected. The histopathological analyses showed an exacerbated inflammation and granulomatous-like infiltrate with the Querétaro strain. Interestingly, extensive calcification areas were observed in the skeletal muscle surrounded by inflammatory infiltrates. TNF-α and IL-10 expression exhibited a significant increase at the peak of infection. In summary, Querétaro strain, a Mexican TcI strain, is virulent enough to induce high inflammation and calcification in skeletal muscle of the hind limbs, which could be related to high expression levels of TNF-α.
Highlights
Chagas disease, an important health problem in Latin America, is the manifestation of tissue damage resulting from infection with the hemoflagellate protozoan parasite, Trypanosoma cruzi
An important difference between both infections was the presence of pale areas observed only on the skeletal muscle of the posterior extremities from the animals infected with the Queretaro strain (Figure 1(c)), as well as loss of muscular mass in the same area
We analyzed the histopathological damage of skeletal muscle from mice caused by the infection with the Mexican TcI strains, Queretaro and Ninoa
Summary
An important health problem in Latin America, is the manifestation of tissue damage resulting from infection with the hemoflagellate protozoan parasite, Trypanosoma cruzi. This parasite constitutes a very heterogenic taxon, allowing the clustering of T. cruzi strains into six discrete typing units (DTUs): TcI to TcVI [1]. In Mexico, it has been reported that 98% of the isolated strains belong to TcI and are closely related to each other [7, 8]; the presence of chronic symptomatic evolutions has been shown [9,10,11], with 5000 people affected with severe chronic chagasic cardiomyopathy [12], indicating that TcI is dominant in Mexico even in human infections
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