A new landscape of host–protozoa interactions involving the extracellular vesicles world

Abstract

Extracellular vesicles (EVs) are released by a wide number of cells including blood cells, immune system cells, tumour cells, adult and embryonic stem cells. EVs are a heterogeneous group of vesicles (~30-1000 nm) including microvesicles and exosomes. The physiological release of EVs represents a normal state of the cell, raising a metabolic equilibrium between catabolic and anabolic processes. Moreover, when the cells are submitted to stress with different inducers or in pathological situations (malignancies, chronic diseases, infectious diseases.), they respond with an intense and dynamic release of EVs. The EVs released from stimulated cells vs those that are released constitutively may themselves differ, both physically and in their cargo. EVs contain protein, lipids, nucleic acids and biomolecules that can alter cell phenotypes or modulate neighbouring cells. In this review, we have summarized findings involving EVs in certain protozoan diseases. We have commented on strategies to study the communicative roles of EVs during host-pathogen interaction and hypothesized on the use of EVs for diagnostic, preventative and therapeutic purposes in infectious diseases. This kind of communication could modulate the innate immune system and reformulate concepts in parasitism. Moreover, the information provided within EVs could produce alternatives in translational medicine.

Extracellular vesicles produced by bone marrow mesenchymal stem cells attenuate renal fibrosis, in part by inhibiting the RhoA/ROCK pathway, in a UUO rat model

“…Emerging data supports that BMSCs exert their positive effect by releasing EVs, which may be more effective. EVs, which are typically approximately 30-1000 nm in size and are composes of exosomes, microvesicles and apoptotic bodies, are membranous bodies that are released by almost all cells [28,29]. EVs attract more attention in the field of organ regeneration because they selectively packed with s proteins, mRNAs, microRNAs, and lipids [30].…”

Trypanosoma cruzi-Infected Human Macrophages Shed Proinflammatory Extracellular Vesicles That Enhance Host-Cell Invasion via Toll-Like Receptor 2

“…It is known that inflammatory responses occur during T. cruzi infection and that this can be reproduced by the parasite EVs (Nogueira et al, 2015). Likewise, Dr Ramirez's group showed that metacyclic-trypomastigotes induce the release of TGF-β coated plasma membrane vesicles from blood macrophages and lymphocytes, which could further increase parasite infectivity (Cestari et al, 2012;Wyllie and Ramirez, 2017;Gavinho et al, 2018;Rossi et al, 2019). However, it is unknown whether EVs released by T. cruzi-infected macrophages or EVs isolated from parasite modulate hotst inflammatory responses and cell invasion.…”

Perils and Promises of Pathogenic Protozoan Extracellular Vesicles

“…Incidentally, simultaneous secretion of exosomes and plasma membrane blebs has been predicted among Leishamania spp (Montaner et al, 2014 ). The biogenesis and classification of exosomes and other EVs have been expertly reviewed in depth by Garcia-Silva et al ( 2014 ), Colombo et al ( 2014 ), and Gavinho et al ( 2018 ). The internal volume of an exosome ranges between 20 and 90 nm 3 with a capacity to lodge an estimated 100 proteins and 10,000 nucleotides, values that should be higher in ectosomes and apoptotic bodies (Torró et al, 2018 ).…”

“…EVs also play important roles as channels of intercellular communication within parasite population (Gavinho et al, 2018 ). Additionally, as suggested by Geiger et al ( 2010 ), T. brucei may possibly use MVs to communicate between trypanosomes by exchanging non-protein cytosolic receptors or genomic information to harness survival strategies.…”