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Published on: September 30, 2017
Surface Molecules Released by Trypanosoma cruzi Metacyclic Forms Downregulate Host Cell Invasion
Tatiana Mordente Clemente1, Cristian Cortez1, Antônio da Silva Novaes2
1Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de São Paulo, São Paulo, Brasil.
Metacyclic trypomastigote (MT) surface molecules gp82 and gp90 are released by T. cruzi strains and can inhibit host cell invasion. Higher release from poorly invasive strains impairs parasite entry, suggesting a regulatory role in infection.
Area of Science:
- Parasitology
- Cell Biology
- Infectious Diseases
Background:
- Trypanosoma cruzi metacyclic trypomastigote (MT) surface molecule release and its impact on host cell invasion are not fully understood.
- T. cruzi strains exhibit varying abilities to invade host cells, necessitating investigation into underlying mechanisms.
Purpose of the Study:
- To investigate differential release of MT surface molecules by T. cruzi strains.
- To determine the effect of released surface molecules on host cell invasion.
Main Methods:
- Incubation of MT forms in different media (D10, PBS++) to collect conditioned media (CM).
- Western blot analysis of CM using antibodies against gp82 and gp90.
- Host cell invasion assays using HeLa cells incubated with CM from different T. cruzi strains.
Main Results:
- Conditioned medium from poorly invasive G strain (G-CM) contained high levels of gp82 and gp90, inhibiting host cell invasion.
- Conditioned medium from highly invasive CL strain (CL-CM) had low levels of these molecules and did not inhibit invasion.
- G-CM's inhibitory effect was neutralized by antibodies against gp82 and gp90.
Conclusions:
- Spontaneously released MT surface molecules, gp82 and gp90, impair parasite-host cell interaction and invasion.
- gp82 may compete for host cell receptors, while gp90 further downregulates invasion.
- Differential release of these molecules by T. cruzi strains influences their invasive potential.
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