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Cardiac alterations induced by Trypanosoma cruzi extracellular vesicles and immune complexes

Alberto Cornet-Gomez1, Francisco O'Valle2,3,4, José M Garrido2,5,6

  • 1Department of Parasitology, Biochemical and Molecular Parasitology Group CTS-183, and Institute of Biotechnology, University of Granada, Granada, Spain.

Plos Neglected Tropical Diseases
|July 7, 2025
PubMed

Insights

Extracellular vesicles (EVs) from Trypanosoma cruzi, forming immune complexes with IgG, induced cardiac damage in mice, mimicking Chagas disease cardiomyopathy. These EVs are identified as potential virulence factors contributing to Chagas disease progression.

Area of Science:

  • Immunology
  • Parasitology
  • Cardiology

Background:

  • Chagas disease (CD), caused by Trypanosoma cruzi, often leads to severe cardiac complications in its chronic phase.
  • The precise mechanisms driving Chagas cardiomyopathy remain incompletely understood, with proposed roles for parasite factors and host immune responses.
  • Extracellular vesicles (EVs) are implicated in parasite-host communication and immune modulation, with emerging potential as diagnostic tools.

Purpose of the Study:

  • To investigate the role of EVs released by Trypanosoma cruzi and their immune complexes (ICs) with anti-T. cruzi IgGs in the development of cardiac alterations.
  • To assess the impact of EVs and ICs on cardiac function, protein expression, and inflammatory markers in a murine model.

Main Methods:

  • Mice were intravenously injected with EVs and ICs (EVs-IgG) over 21 days.
  • Evaluated autoantibody presence, electrocardiography (ECG), cardiac histopathology, and protein and cytokine expression in the heart.
  • Measured serum B-type natriuretic peptide (BNP) levels.

Main Results:

  • EVs and ICs induced ECG alterations, including changes in heart rate and PR interval.
  • Cardiac structural changes and reduced expression of key proteins (connexin 43, tubulin, dynein) were observed.
  • VCAM-1 expression was altered, cytokine profiles in the heart changed, and serum BNP levels increased, indicating cardiac damage.

Conclusions:

  • EVs shed by Trypanosoma cruzi and the immune complexes they form with IgG can induce cardiac alterations similar to those in Chagas disease.
  • This study underscores the significant role of EVs in Chagas disease pathogenicity.
  • EVs should be considered critical virulence factors in the development and progression of Chagas disease.
Abstract

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