Extracellular Vesicles in Trypanosomatids: Host Cell Communication.

Ana Claudia Torrecilhas,Martin Olivier,Christopher Fernández-Prada,Sergio Schenkman,Rodrigo Pedro Soares

doi:10.3389/fcimb.2020.602502

Abstract

Trypanosoma cruzi, Trypanosoma brucei and Leishmania (Trypanosomatidae: Kinetoplastida) are parasitic protozoan causing Chagas disease, African Trypanosomiasis and Leishmaniases worldwide. They are vector borne diseases transmitted by triatomine bugs, Tsetse fly, and sand flies, respectively. Those diseases cause enormous economic losses and morbidity affecting not only rural and poverty areas but are also spreading to urban areas. During the parasite-host interaction, those organisms release extracellular vesicles (EVs) that are crucial for the immunomodulatory events triggered by the parasites. EVs are involved in cell-cell communication and can act as important pro-inflammatory mediators. Therefore, interface between EVs and host immune responses are crucial for the immunopathological events that those diseases exhibit. Additionally, EVs from these organisms have a role in the invertebrate hosts digestive tracts prior to parasite transmission. This review summarizes the available data on how EVs from those medically important trypanosomatids affect their interaction with vertebrate and invertebrate hosts.

Highlights

Trypanosoma cruzi and Chagas’ DiseaseAmerican trypanosomiasis, popularly known as Chagas’ disease (CD), whose etiologic agent is the flagellated protozoan Trypanosoma cruzi was first described by Carlos Chagas in 1909
We identified other proteins related to exosomes and vacuoles, such as heat-shock protein 85 (HSP85), elongation factor 1-alpha, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), vacuolar ATP synthase subunit B, and tetratric-peptide-repeat (TPR) protein (Théry et al, 2018; Doyle and Wang, 2019)
Using GP63-deficient Leishmania major parasites, we demonstrated that the absence of this virulence factor, which is greatly enriched in wild-type L. major exosomes, was almost completely abrogating their capacity to modulate host immune response comparatively to its wild-type counterpart (Hassani et al, 2014)

Summary

Introduction

Trypanosoma cruzi and Chagas’ DiseaseAmerican trypanosomiasis, popularly known as Chagas’ disease (CD), whose etiologic agent is the flagellated protozoan Trypanosoma cruzi was first described by Carlos Chagas in 1909. EVs isolated from T. cruzi trypomastigotes derived from mammalian cells contain most of the parasite cell-surface proteins, including major surface glycoproteins that resemble to mucins (Ribeiro et al, 2018) (Table 1).

Results

Conclusion