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Complementary surface epitopes, myotropic adhesion and active grip in Trypanosoma cruzi-host cell recognition
B F von Kreuter1, M Sadigursky, C A Santos-Buch
1Department of Pathology, Cornell University Medical College, New York, NY 10021.
Molecular and Biochemical Parasitology
|September 1, 1988
Summary
Trypanosoma cruzi parasites preferentially adhere to L6 myoblast host cells via specific surface molecules. This adhesion process involves calcium ions and energy-dependent mechanisms, indicating an active binding interaction.
Area of Science:
- Cell biology
- Parasitology
- Molecular interactions
Background:
- Trypanosoma cruzi (T. cruzi) is a protozoan parasite that causes Chagas disease.
- Understanding T. cruzi adhesion mechanisms is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the preferential adhesion of T. cruzi to specific host cells.
- To elucidate the molecular mechanisms underlying T. cruzi-host cell interactions.
Main Methods:
- Studying the adhesion of T. cruzi metacyclic trypomastigotes and epimastigotes to L6 myoblast, smooth muscle, and epithelial cells.
- Analyzing adhesion as a function of time, surface area, and concentration at different temperatures (4°C and 37°C).
- Investigating the role of calcium ions and energy-dependent processes in adhesion.
Main Results:
- T. cruzi parasites showed preferential adhesion to L6 myoblast cells compared to smooth muscle and epithelial cells.
- Adhesion exhibited saturation kinetics, dependent on time, surface area, and concentration.
- Initial adhesion rates were partially calcium-dependent.
- At saturation, adhesion depended on high-energy phosphorylated intermediates, suggesting an active binding mechanism.
Conclusions:
- T. cruzi possesses surface molecules that bind to complementary receptors on L6 myoblast host cells.
- The adhesion process is an active, energy-dependent mechanism involving calcium ions.
- These findings support the existence of specific parasite attachment molecules and host cell receptors.