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Related Experiment Video

Updated: May 5, 2026

Establishment of Larval Zebrafish as an Animal Model to Investigate Trypanosoma cruzi Motility In Vivo

Establishment of Larval Zebrafish as an Animal Model to Investigate Trypanosoma cruzi Motility In Vivo

Published on: September 30, 2017

Endothelial transmigration by Trypanosoma cruzi.

Bria M Coates¹, David P Sullivan, Ming Y Makanji

¹Departments of Pediatrics and Pathology, Northwestern University, Chicago, Illinois, United States of America.

|December 7, 2013

Summary

Trypanosoma cruzi, the parasite causing Chagas heart disease, can rapidly cross the endothelial barrier without causing infection or damaging blood vessels. Bradykinin and CCL2 enhance this parasite transmigration.

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Last Updated: May 5, 2026

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Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs

Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs

Published on: June 23, 2022

Area of Science:

Parasitology
Cardiovascular Disease Research
Cell Biology

Background:

Chagas heart disease, a major cause of heart failure in Latin America, stems from Trypanosoma cruzi infection.
The mechanism by which T. cruzi crosses the endothelial barrier to infect tissues from the bloodstream remains largely undescribed.
Understanding T. cruzi-endothelial interactions is crucial for developing therapies against Chagas disease pathogenesis.

Purpose of the Study:

To investigate the transmigration of T. cruzi across endothelial cells in vitro.
To identify factors that facilitate parasite dissemination through the vascular endothelium.
To explore novel therapeutic targets for Chagas disease.

Main Methods:

Adapted leukocyte transmigration assays to study T. cruzi interaction with endothelial cells.
Utilized in vitro models to observe and quantify parasite migration across endothelial monolayers.
Investigated the role of bradykinin and the chemokine CCL2 in parasite transmigration.

Main Results:

Provided the first evidence of rapid T. cruzi transmigration across endothelial cells.
Demonstrated that transmigration is distinct from productive infection and does not compromise endothelial barrier integrity.
Identified bradykinin as a facilitator and CCL2 as an enhancer of T. cruzi transmigration.

Conclusions:

T. cruzi can efficiently cross the endothelial barrier via a non-infectious, non-disruptive mechanism.
Bradykinin and CCL2 play significant roles in facilitating parasite dissemination.
These findings offer new insights into Chagas disease pathogenesis and potential therapeutic strategies.