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Gene expression profiles in response to Fas stimulation in Trypanosoma cruzi-infected host cells
Muneaki Hashimoto1, Junko Nakajima-Shimada, Kazumi Ishidoh
1Department of Molecular and Cellular Parasitology, Juntendo University School of Medicine, 2-1-1, Hongo, Tokyo 113-8421, Japan.
Abstract:
To determine the molecular mechanism by which apoptosis is inhibited in Trypanosoma cruzi-infected host cells, we used human cDNA apoptosis chips to compare the gene expression profiles in response with 'death ligands target' (Fas) stimulation in infected and uninfected cells. Of the 164 apoptosis-related genes examined, 20, including those encoding both pro- and anti-apoptotic proteins, were highly up-regulated in the infected group. Genes encoding caspases and apoptosis inhibitors were optimally expressed 10-30 min after induction of apoptosis, whereas genes involved in transcriptional regulation and cell proliferation were up-regulated after 2-24 h. These results suggest that host anti-apoptotic gene(s) may play a crucial role in the inhibition of Fas-mediated apoptosis in T. cruzi-infected cells.
Insights
Trypanosoma cruzi infection inhibits host cell apoptosis by up-regulating specific anti-apoptotic genes. These host genes play a crucial role in preventing programmed cell death during infection.
Area of Science:
- Molecular Biology
- Cell Biology
- Parasitology
Background:
- Trypanosoma cruzi infection can alter host cell processes.
- Understanding host-pathogen interactions is crucial for disease control.
- Apoptosis is a key cellular process often manipulated by pathogens.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying apoptosis inhibition in T. cruzi-infected host cells.
- To identify specific host genes involved in preventing Fas-mediated apoptosis.
Main Methods:
- Utilized human cDNA apoptosis chips for gene expression profiling.
- Compared gene expression in infected versus uninfected host cells upon Fas stimulation.
- Analyzed the temporal expression patterns of apoptosis-related genes.
Main Results:
- Out of 164 apoptosis-related genes, 20 were significantly up-regulated in infected cells.
- Both pro- and anti-apoptotic protein-encoding genes showed increased expression.
- Caspaes and apoptosis inhibitor genes peaked at 10-30 minutes post-induction.
- Transcriptional regulation and cell proliferation genes were upregulated later (2-24 hours).
Conclusions:
- Host anti-apoptotic gene(s) are likely critical in inhibiting Fas-mediated apoptosis in T. cruzi-infected cells.
- T. cruzi manipulates host gene expression to promote cell survival.
- This study provides insights into the host-pathogen molecular interplay during Chagas disease pathogenesis.
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