Infecção de células epiteliais com diferentes populações de Trypanosoma cruzi: análise da ação do fator de necrose tumoral

Abstract

Trypanosoma cruzi, the etiologic agent of Chagas disease, is able to enter into all cell types of mammalian cells. The infection is a process dependent on various factors such as the glycoproteins present on the surface of the parasite and the target cell, the population of T. cruzi and cell signaling triggered by parasite-target cell interaction. It is known that, in experimental models, the pathological and immunological profile of the infection depends on the population of T. cruzi. In this work, we aimed to examine whether the pro-inflammatory cytokine TNF-alpha has an effect on epithelial cell invasion by trypomastigotes of two populations of T. cruzi belonging to different DTU (Discrete Typing Units). We have also investigated whether the infected cells show any ultrastructural changes after 22 hours of infection. Our results show that epithelial LLC-MK2 cells and HEK293 cells are more susceptible to infection by Col1.7G2 clone, which belongs to the DTU/TCI class compared with infection by clone CL-Brener, which belongs to TCVI. In relation to clone CL-Brener, HEK293 cells are more susceptible to infection than the LLC-MK2 cells. Our data also show that, contrary to the previously findings with strain Y, TNF-alpha had no effect on the proportions of infected cells and the number of intracellular parasites in both cell types studied. Interestingly, analysis by transmission electron microscopy indicates that mitochondria of epithelial cells tend to accumulate around the parasite, often in close juxtaposition to its plasma membrane, during the period of 22 hours of infection. These data demonstrate the complexity of the invasion process, which proved to be dependent on the cell type and the population of the parasite. Thus, further studies will be important for clarify the molecules involved in this process as well as the involvement of mitochondria in the infection and maintenance of the parasite in the host cell.