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Early Trypanosoma cruzi infection reprograms human epithelial cells
María Laura Chiribao1, Gabriela Libisch2, Adriana Parodi-Talice3
1Unidad de Biología Molecular, Montevideo 11400, Institut Pasteur de Montevideo, Uruguay ; Departamento de Bioquímica, Facultad de Medicina, Universidad de la República, Montevideo 11300, Uruguay.
Biomed Research International
|May 10, 2014
Summary
Trypanosoma cruzi reprograms human epithelial cells upon infection, altering cellular stress, transcription factors, and metabolism. This early host cell reprogramming is crucial for parasite invasion and systemic spread in Chagas disease.
Area of Science:
- Parasitology
- Cell Biology
- Molecular Biology
Background:
- Trypanosoma cruzi causes Chagas disease, a complex parasitic illness.
- T. cruzi's ability to invade diverse cell types complicates treatment and prevention.
- Focus has been on macrophage and cardiomyocyte responses, neglecting initial host barriers.
Purpose of the Study:
- Investigate the early host cell response to T. cruzi infection in human epithelial cells.
- Identify host cellular factors involved in T. cruzi invasion.
- Understand the initial steps of Chagas disease pathogenesis.
Main Methods:
- Transcriptomic analysis of human epithelial cells following T. cruzi infection.
- Identification of significantly altered genes.
- Global gene expression profiling.
Main Results:
- Over 1700 genes were significantly altered upon T. cruzi infection.
- T. cruzi infection induced reprogramming of cellular stress responses, including neutrophil chemotaxis and DNA damage.
- Infection affected numerous transcription factors, notably NF-κB family members, and host metabolism (cholesterol, fatty acids, phospholipids).
Conclusions:
- T. cruzi extensively reprograms host epithelial cells during the early stages of infection.
- This reprogramming impacts cellular stress, transcription, and metabolism, facilitating parasite entry.
- Early host cell manipulation by T. cruzi is key for establishing infection and systemic dissemination.
