ArticleBMC genomics2009
Cytokine-dependent and-independent gene expression changes and cell cycle block revealed in Trypanosoma cruzi-infected host cells by comparative mRNA profiling.
Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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38 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Pooled it
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- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Paracrine Signaling Mediated by the Cytosolic Tryparedoxin Peroxidase ofPathogens (Basel, Switzerland) · 2024Article
- Impact of Laboratory-Adapted IntracellularMicroorganisms · 2023Article
- Unrevealing the Mystery of Latent Leishmaniasis: What Cells Can HostPathogens (Basel, Switzerland) · 2023Review
- Review
- Different Transcriptomic Response toFrontiers in cellular and infection microbiology · 2022Article
- Differential gene expression identifies a transcriptional regulatory network involving ER-alpha and PITX1 in invasive epithelial ovarian cancer.BMC cancer · 2021Article
- DNA damage and oxidative stress in human cells infected by Trypanosoma cruzi.PLoS pathogens · 2021Article
- Article
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Transcriptome analysis of alternative splicing in the pathogen life cycle in human foreskin fibroblasts infected with Trypanosoma cruzi.Scientific reports · 2020Article
- Gene expression network analyses during infection with virulent and avirulent Trypanosoma cruzi strains unveil a role for fibroblasts in neutrophil recruitment and activation.PLoS pathogens · 2020Article
- Besnoitia besnoiti-driven endothelial host cell cycle alteration.Parasitology research · 2020Article
- Investigation of pyrimidine nucleoside analogues as chemical probes to assess compound effects on the proliferation of Trypanosoma cruzi intracellular parasites.PLoS neglected tropical diseases · 2020Article
- Article
- DNA lesions and repair in trypanosomatids infection.Genetics and molecular biology · 2020Article
- Toxoplasma gondii-induced host cellular cell cycle dysregulation is linked to chromosome missegregation and cytokinesis failure in primary endothelial host cells.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe requirements for growth and survival of the intracellular pathogen Trypanosoma cruzi within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by T. cruzi infection of phenotypically diverse human cell types.
resultsWe report significant changes in transcript abundance in T. cruzi-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change > or = 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in T. cruzi-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in T. cruzi-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that T. cruzi infection may impede host cell cycle progression. The observation of impaired cytokinesis in T. cruzi-infected cells, following nuclear replication, confirmed this prediction.
conclusionMetabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to T. cruzi infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of T. cruzi metabolic requirements or effects on the host. However, our methods also revealed a T. cruzi-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.
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