Influência das proteínas ARP2, Septina 4 e 14 na invasão e multiplicação de Trypanosoma cruzi

Abstract

Trypanosoma cruzi, which causes Chagas Disease, is a parasite that uses multiple signaling pathways in the cell for invasion. One of these pathways involves the participation of the actin cytoskeleton in the host cell, which can be an important regulatory factor in infection, which facilitates or prevents the spread of the parasite. Several proteins are associated in this process. It is known that a protein called P21 T. cruzi (Silva et al., 2009) operates by activating a signaling cascade that culminates in the internalization of the parasite. Invasion assays with recombinant His6-P21 protein has shown that this protein induces phagocytic process promoting local actin polymerization in host cells (Rodrigues et al. 2012). This study aimed to verify the involvement of proteins in T. cruzi infection. To this end, tests of invasion and multiplication of the parasite in knockdown cells for Arp2, Septina4 and Septina14 proteins were performed. Cells were also treated with P21-His6 to evaluate the role of these proteins in actin polymerization. It was observed that at certain times the significant reduction of invasion or multiplication of Arp2 and Septins 4 and 14, enable the progression of the infection, since the number of parasites in knockdown cells showed a significant increase compared to the control group. Thus arises the hypothesis that the proteins analyzed could function as an apparatus that prevents or decreases the invasion / multiplication of the parasite. In actin polymerization assays, it was observed that the Arp2 septin 14 and part of the protein via the activated P21 to induce such an effect. Correlating all results obtained in this study, a possible importance of Arp2 and septin 14 protein in the process of becoming chronic Chagas disease can be questioned. Overall, the results show the importance of the proteins studied here as possible targets of intervention to control or inhibit infection by T. cruzi.