Mammalian Target of Rapamycin Inhibition in Trypanosoma cruzi-Infected Macrophages Leads to an Intracellular Profile That Is Detrimental for Infection

ROJAS MÁRQUEZ, JORGE DAVID; ANA, YAMILE; BAIGORRÍ, RUTH ELIANA; STEMPIN, CINTHIA CAROLINA; CERBAN, FABIO MARCELO

Frontiers in Immunology

Frontiers editorial

Lugar: Lausanne; Año: 2018 vol. 9

he causative agent of Chagas? disease, Trypanosoma cruzi, affects approximately10 million people living mainly in Latin America, with macrophages being one of thefirst cellular actors confronting the invasion during T. cruzi infection and their functiondepending on their proper activation and polarization into distinct M1 and M2 subtypes.Macrophage polarization is thought to be regulated not only by cytokines and growthfactors but also by environmental signals. The metabolic checkpoint kinase mammaliantarget of rapamycin (mTOR)-mediated sensing of environmental and metabolic cuesinfluences macrophage polarization in a complex and as of yet incompletely understoodmanner. Here, we studied the role of the mTOR pathway in macrophages during T. cruziinfection. We demonstrated that the parasite activated mTOR, which was beneficial forits replication since inhibition of mTOR in macrophages by different inhibitors decreasedparasite replication. Moreover, in rapamycin pretreated and infected m