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Molecular Mechanisms of Parasitic Diseases

Special Issue Editor


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Guest Editor
Faculdade de Medicina, Universidade Nilton Lins, Manaus 69058030, Amazonas, Brazil
Interests: parasite; immunology

Special Issue Information

Dear Colleagues,

Genetic studies in animal models of infection and human infectious diseases may provide a deeper biological understanding of why only a fraction of infected individuals progress to clinical disease, while the majority generally remain asymptomatic. What constitutes protective immunity? Studying human genetics in the context of infectious diseases may elucidate the mechanism underlying protective immune responses. While it is known that the presence of a pathogen is necessary to trigger disease, the genetic basis underlying interindividual susceptibility remains poorly understood in most infectious diseases. For this Special Issue, “Molecular Mechanisms of Parasitic Diseases”, we invite the submission of manuscripts that investigate the pathogenesis of parasitic infections at both the cellular and host levels. Studies focusing on cellular biology, animal models and clinical investigations and examining the determinants of parasitic disease progression are welcome. We also encourage the submission of human genetic and immunological studies on the mechanisms causing only a subset of individuals to develop symptomatic parasitic infections, despite widespread exposure.

Dr. Rajendranath Ramasawmy
Guest Editor

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Keywords

  • parasites
  • molecular mechanisms
  • pathogenesis
  • genetics
  • symptomatics

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Published Papers (1 paper)

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Research

16 pages, 2013 KB  
Article
Placental Barrier Breakdown Induced by Trypanosoma cruzi-Derived Exovesicles: A Role for MMP-2 and MMP-9 in Congenital Chagas Disease
by Alejandro Fernández-Moya, Ana Liempi, Marioly Müller, Rocío Arregui, Antonio Osuna, Alberto Cornet-Gómez, Christian Castillo and Ulrike Kemmerling
Int. J. Mol. Sci. 2025, 26(24), 12131; https://doi.org/10.3390/ijms262412131 - 17 Dec 2025
Viewed by 494
Abstract
Trypanosoma cruzi, the causative agent of Chagas disease, can cross the placental barrier and be transmitted congenitally, yet the mechanisms underlying this process remain incompletely understood. Recent evidence suggests that T. cruzi-derived extracellular vesicles (TcEVs) may facilitate placental invasion by modulating [...] Read more.
Trypanosoma cruzi, the causative agent of Chagas disease, can cross the placental barrier and be transmitted congenitally, yet the mechanisms underlying this process remain incompletely understood. Recent evidence suggests that T. cruzi-derived extracellular vesicles (TcEVs) may facilitate placental invasion by modulating host–pathogen interactions. In this study, we examined the effects of TcEVs on human placental explants (HPEs), focusing on their capacity to disrupt tissue architecture and modulate matrix metalloproteinases MMP-2 and MMP-9, enzymes critical for extracellular matrix remodeling. Term placental chorionic villi were cultured ex vivo and exposed to TcEVs, heat-inactivated TcEVs, infective trypomastigotes, or combinations thereof. TcEVs induced ultrastructural damage, including trophoblast detachment and basal lamina disorganization, which were exacerbated by co-incubation with parasites. Immunohistochemistry and Western blotting revealed significant upregulation of MMP-2 and MMP-9, while gelatin zymography confirmed increased enzymatic activity. Our findings demonstrate that TcEVs independently and synergistically with T. cruzi compromise placental integrity by enhancing MMP expression and activity, thereby priming the placental microenvironment for parasite invasion. Targeting TcEVs signaling or MMP activation may represent a novel strategy to prevent congenital transmission of T. cruzi. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Parasitic Diseases)
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