Review on Trypanosoma cruzi: Host Cell Interaction

Figure 10

Model of T. cruzi invasion. The model indicates three distinct mechanisms of T. cruzi entry into host cell. (a) the lysosome-dependent pathway is initiated by targeted Ca²⁺-regulated exocytosis of lysosomes in the plasma membrane; (b) in the actin dependent pathway trypomastigotes penetrate into a host cell through a plasma membrane expansion that culminates in assembly of a parasitophorous vacuole. Either learly endosomes or lysosomes can fuse with the parasitophorous vacuole; (c) in the lysosome-independent pathway, parasites enter cells through plasma membrane invaginations that accumulate PIP₃ (product of class I PI3K activation). Subsequently, internalized parasites are contained in vacuoles formed from the plasma membrane and it maturates with the acquisition of early endosome markers (rab5 and EEA1) and subsequently with the acquisition of lysosome markers. Later on, the the trypomastigote form gradually transform into a amastigote form with simultaneous lysis of the parasitophorous vacuole membrane. Then, amastigotes in direct contact with the cytoplasm start to divide.