EFFECT OF DRUGS THAT MODULATE AUTOPHAGY ON

VANRELL MC, CASASSA AF, COLOMBO MI, ROMANO PS

Mendoza

Otro; XXVIII Annual Scientific Meeting of the CUYO BIOLOGY SOCIETY; 2011

Trypanosoma cruzi, the etiologic agent of Chagas disease, adopts different forms during its biologic cycle. In the gut of the vector, different forms during its biologic cycle. In the gut of the vector, different forms during its biologic cycle. In the gut of the vector, different forms during its biologic cycle. In the gut of the vector, different forms during its biologic cycle. In the gut of the vector, different forms during its biologic cycle. In the gut of the vector, the etiologic agent of Chagas disease, adopts different forms during its biologic cycle. In the gut of the vector, Triatoma infestans, the replicative epimastigote form (E) differentiates to infective metacyclic trypomastigotes (MT). Trypomastigotes can invade a wide range of nucleated cells, changing to the amastigote form (A) in the cytosol of host cells. Amastigotes are the intracellular replicative forms indispensable to continue the cycle. Although the mechanisms that govern these changes are poorly understood, it is accepted that starvation is a key stimulus for the E to MT differentiation. Autophagy is an intracellular process mainly activated during nutrient deprivation. We have studied the effect of drugs or conditions that regulate autophagy during E to MT (or T to A) T. cruzi differentiation. Using E from the GFP-Y strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi to infective metacyclic trypomastigotes (MT). Trypomastigotes can invade a wide range of nucleated cells, changing to the amastigote form (A) in the cytosol of host cells. Amastigotes are the intracellular replicative forms indispensable to continue the cycle. Although the mechanisms that govern these changes are poorly understood, it is accepted that starvation is a key stimulus for the E to MT differentiation. Autophagy is an intracellular process mainly activated during nutrient deprivation. We have studied the effect of drugs or conditions that regulate autophagy during E to MT (or T to A) T. cruzi differentiation. Using E from the GFP-Y strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi to infective metacyclic trypomastigotes (MT). Trypomastigotes can invade a wide range of nucleated cells, changing to the amastigote form (A) in the cytosol of host cells. Amastigotes are the intracellular replicative forms indispensable to continue the cycle. Although the mechanisms that govern these changes are poorly understood, it is accepted that starvation is a key stimulus for the E to MT differentiation. Autophagy is an intracellular process mainly activated during nutrient deprivation. We have studied the effect of drugs or conditions that regulate autophagy during E to MT (or T to A) T. cruzi differentiation. Using E from the GFP-Y strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi strain, we have observed that treatment with the autophagy inhibitor Wortmannin (200 nM) reduces the percentage of MT recovered during in vitro differentiation, as indicated by a reduction in the percentage of infected cells and number of parasites/cell. Conversely, the differentiation from T to A was significantly increased when the parasites were submitted to starvation or to the autophagy inductor Rapamycin (50 ng/ml). These results indicate that autophagy is a pathway that actively participates during the T. cruzi percentage of infected cells and number of parasites/cell. Conversely,