Abstract
Trypanosoma cruzi is an obligatory intracellular protozoan parasite, and it is the etiological agent of Chagas’ disease that is endemic in the Americas. In addition to humans, a wide spectrum of mammals can be infected by T. cruzi, including dogs. Dogs develop acute and chronic disease, similar to human infection. T. cruzi can infect almost all cell types and after cell invasion, the metacyclics trypomastigotes localize in the cytoplasm, where they transform into amastigotes, the replicative form of T. cruzi in mammals. After amastigote multiplication and differentiation, parasites lyse host cells and spread through the body by blood circulation. In this work, we evaluated the in vitro ability of T. cruzi to infect a canine macrophage cell line DH82 compared with RAW264.7, a murine tissue culture macrophage. Our results have shown that the T. cruzi is able to infect, replicate and differentiate in DH82 cell line. We observed that following treatment with LPS and IFN-γ DH82 cells were more resistant to infection and that resistance was not related reactive oxygen species production in our system. In this study, we also found that DH82 cells became more susceptible to T. cruzi infection when cocultured with apoptotic cells. The analysis of cytokine production has showed elevated levels of the TGF-β, IL-10, and TNF-α produced by T. cruzi-infected canine macrophages. Additionally, we demonstrated a reduced expression of the MHC class II and CD80 by infected DH82 cell line.
Highlights
Chagas’ disease is caused by the protozoan hemoflagellate Trypanosoma cruzi, which is transmitted by a blood-sucking reduviid bugs [1]
To further confirm DH82 macrophage cell line infection, we have used T. cruzi of CL strain transfected with green fluorescent protein (GFP) and observed the adhesion, internalization and differentiation into intracellular amastigotes 5 days after infection (Figure 1C)
For the first time, that the DH82, a canine macrophage cell line is susceptible to infection with T. cruzi, being able to provide an enabling environment for replication and differentiation of the parasite and the release of viable infective forms
Summary
Chagas’ disease is caused by the protozoan hemoflagellate Trypanosoma cruzi, which is transmitted by a blood-sucking reduviid bugs [1]. It was described more than 100 years ago, this disease remains a serious public health problem in South and Central America countries, which come to account for 12 million to 14 million of infected people [2]. The T. cruzi infection begins when the infective metacyclic trypomastigotes forms are transmitted to humans or other mammals by the infected feces of triatomine bugs. After cell invasion trypomastigotes transform into amastigotes, that multiply. After reaching the bloodstream and lym phatic vessels, blood trypomastigotes can invade other tissues, penetrate the cells, and differentiate again into amastigotes, forming new multiplying foci. There is a latent phase of infection, called indeterminate phase, which can last for long periods of time or can be permanent, develops into a chronic stage [3]
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