Stress Induces Release of Extracellular Vesicles by Trypanosoma cruzi Trypomastigotes

Journal of Immunology Research, 2021 · DOI: https://doi.org/10.1155/2021/2939693 · Published: September 24, 2021

Simple Explanation

Trypanosoma cruzi, the parasite causing Chagas disease, releases vesicles containing surface molecules. This release is affected by environmental conditions. This study investigates how stress conditions impact this vesicle release and whether it alters their immunomodulatory properties. The research shows that low temperatures and acidic conditions increase vesicle release, while certain chemicals reduce it. These vesicles can be reabsorbed by the parasites. Stress conditions do not change the pro-inflammatory activity of these vesicles on macrophages. The findings suggest that vesicle release depends on the parasite's membrane structure and its integrity. Variations in vesicle release under stress may be a defense mechanism against environmental changes encountered by the parasite.

Study Duration

Not specified

Participants

6- to 8-week-old female C57Bl/6 mice for Bone Marrow-Derived Macrophage

Evidence Level

Not specified

Key Findings

1
Low temperatures (4°C) and acidic conditions (pH 5.0) increase EV release by Trypanosoma cruzi trypomastigotes.
2
Sodium azide and methyl-cyclo-β-dextrin (CBD) reduce EV release, indicating the importance of membrane organization for this process.
3
Nitrosative stress, induced by sodium nitrite in acidic medium or S-nitrosoglutathione, stimulates the secretion of EVs.

Research Summary

This study investigates the impact of various stress conditions on the release of extracellular vesicles (EVs) by Trypanosoma cruzi trypomastigotes. The research examines how factors like temperature, pH, and chemical agents affect EV release and whether these stress conditions alter the immunomodulatory properties of the released EVs. The key findings indicate that EV release is influenced by membrane structure and parasite integrity. Specifically, low temperatures and acidic conditions promote EV release, while certain chemical inhibitors reduce it. Nitrosative stress also stimulates EV secretion. The EVs released under these varying conditions maintain their pro-inflammatory activity. The study concludes that the variations in EV release under stress conditions may represent a physiological response by the parasite to environmental changes. The findings suggest a budding mechanism of release that depends on membrane organization.

Practical Implications

Drug Development

Targeting EV release mechanisms could be a novel approach for controlling Trypanosoma cruzi infection.

Understanding Parasite Survival

Understanding how stress influences EV release can shed light on the parasite's survival strategies in different host environments.

Immunomodulation Strategies

Given the pro-inflammatory role of EVs, modulating their release or content could be explored as a way to influence the host immune response during Chagas disease.

Study Limitations

1
The study primarily focuses on in vitro experiments, limiting direct translation to in vivo conditions.
2
The specific molecular mechanisms governing stress-induced EV release remain to be fully elucidated.
3
The long-term effects of stress-induced EV release on the progression of Chagas disease are not explored.

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