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The role of AKT1 and Akt2 signaling during Trypanosoma cruzi infection

Grant number: 13/24312-1
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): March 13, 2014
Effective date (End): December 17, 2014
Field of knowledge:Biological Sciences - Immunology - Cellular Immunology
Principal researcher:Thiago Mattar Cunha
Grantee:Maria Cláudia da Silva
Supervisor abroad: Christos Tsatsanis
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: University of Crete, Heraklion (UoC), Greece  
Associated to the scholarship:11/09488-0 - Investigation of the mechanisms involved in the susceptibility to Trypanosoma cruzi infection in phosphatidylinositol 3-kinase gamma (PI3Kgama) deficient mouse, BP.DR


Chagas disease, caused by infection with the protozoan Trypanosoma cruzi (T. cruzi), is an important cause of heart disease in Latin America, where is endemic. After recognition by immune cells, parasite activates several intracellular signals including activation of phosphatidylinositol 3-kinases (PI3Ks) signaling. When it occurs, PI3K pathway activates, among others downstream signaling, a family of serine/threonine protein kinases named Akt. Members of this family, Akt1, Akt2 and Akt3 are differently expressed in several tissues, playing diverse cellular activities. Recent studies demonstrated that Akt1 and Akt2 are involved in different profiles of macrophages differentiation, such as M2 and M1 respectively. Previews results from our laboratory have shown that, during T. cruzi infection, the host PI3K-gamma activation and Akt phosphorylation are essential to confer resistance. Moreover, the lack of PI3K-gamma signaling seems to modulate macrophage activity against T. cruzi infection, however, there is no study appointing the role of different Akt isoforms during this infection. So, in this project, we intend to investigate the individual role of the protein kinases Akt1 and Akt2 in the heart inflammation caused by T. cruzi infection. Specifically, we will evaluate which AKT (Akt1 or Akt2) is coupled to PI3K-gamma signaling during T. cruzi infection that can influence macrophages profile infiltrating the heart. This study will contribute to a better comprehension of the molecular mechanism that account for susceptibility/resistance to Chagas disease. (AU)

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