The Dialogue of the Host-Parasite Relationship: Leishmania spp. and Trypanosoma cruzi Infection

Figure 3

General molecular mechanisms for host cell invasion by Trypanosoma cruzi. (1) Several receptor-ligand complexes seem to participate in T. cruzi internalization by the host cell. The enzyme transsialidase transfers sialic acid from host cell membrane to Tc-mucins. These molecules can interact with host cell receptor. Some host cell receptors remain unknown. Glycoproteins from the parasite (gp 83 and gp 85, resp.) can bind to host cell receptors, such as P74 or EMCP. Members of Tc85 family can bind to specific receptor (SR) promoting cytoskeletal changes and facilitate parasite invasion. (2) During the process, the host cell adenylate cyclase is activated promoting an enhancement of AMPc that contributes to Ca²⁺ release from endoplasmic reticulum. (3) The cruzipain secreted by the parasite cleaves the host kininogen to liberate bradykinin, and the triggering of the host bradykinin receptor activates host cell PLC, contributing to Ca²⁺ release, via IP₃. (4) Ca²⁺ seems to promote recruitment of perinuclear lysosomes that contributes to formation of the parasitophorous vacuole. In addition, Ca²⁺ promotes disorganization of actin cytoskeleton, and invasion is facilitated by disruption of microfilaments. (5) In another route, the parasite enters into host cell by creating an invagination in the plasma membrane, which accumulates PIP3. (6) After the PV formation, TcTox promotes pores in their membrane and the trypomastigotes escape for cytoplasm. (7) Trypomastigotes transform into amastigotes, multiplying inside the cytoplasm from host cell. N—nucleus, PV—parasitophorous vacuole.