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EXTRACELLULAR VESICLES: POTENTIAL ROLE IN REMOTE SIGNALING AND INFLAMMATION IN TRYPANOSOMA CRUZI-TRIGGERED DISEASE
Vesículas extracelulares
Inflamação
Resposta imune
Trypanosoma cruzi
Affilliation
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia das Interações. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia das Interações. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia das Interações. Rio de Janeiro, RJ, Brasil.
Abstract
Extracellular vesicles (EVs) act as cell communicators and immune response modulators
and may be employed as disease biomarkers and drug delivery systems. In infectious
diseases, EVs can be released by the pathogen itself or by the host cells (infected or
uninfected), potentially impacting the outcome of the immune response and pathological
processes. Chagas disease (CD) is caused by infection by the protozoan Trypanosoma
cruzi and is the main cause of heart failure in endemic areas. This illness attracted
worldwide attention due to the presence of symptomatic seropositive subjects in North
America, Asia, Oceania, and Europe. In the acute phase of infection, nonspecific signs, and
symptoms contribute to miss diagnosis and early etiological treatment. In this phase, the
immune response is crucial for parasite control; however, parasite persistence,
dysregulated immune response, and intrinsic tissue factors may contribute to the
pathogenesis of chronic CD. Most seropositive subjects remain in the indeterminate
chronic form, and from 30 to 40% of the subjects develop cardiac, digestive, or cardiodigestive
manifestations. Identification of EVs containing T. cruzi antigens suggests that
these vesicles may target host cells and regulate cellular processes and the immune
response by molecular mechanisms that remain to be determined. Parasite-released EVs
modulate the host-parasite interplay, stimulate intracellular parasite differentiation and
survival, and promote a regulatory cytokine profile in experimental models of CD. EVs
derived from the parasite-cell interaction inhibit complement-mediated parasite lysis,
allowing evasion. EVs released by T. cruzi-infected cells also regulate surrounding
cells, maintaining a proinflammatory profile. After a brief review of the basic features of
EVs, the present study focuses on potential participation of T. cruzi-secreted EVs in cell
infection and persistence of low-grade parasite load in the chronic phase of infection. We
also discuss the role of EVs in shaping the host immune response and in pathogenesis and
progression of CD.
Keywords in Portuguese
Doença de ChagasVesículas extracelulares
Inflamação
Resposta imune
Trypanosoma cruzi
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