ArticleBioMed research international2014
Early Trypanosoma cruzi infection reprograms human epithelial cells.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Monocyte-derived extracellular vesicles, stimulated by Trypanosoma cruzi, enhance cellular invasion in vitro via activated TGF-β1.Journal of extracellular vesicles · 2024Article
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease.PLoS pathogens · 2024Review
- Paracrine Signaling Mediated by the Cytosolic Tryparedoxin Peroxidase ofPathogens (Basel, Switzerland) · 2024Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Comparative microRNA profiling ofFrontiers in cellular and infection microbiology · 2023Article
- Cellular Stress and Senescence Induction duringTropical medicine and infectious disease · 2022Review
- The cytosolic tryparedoxin peroxidase from Trypanosoma cruzi induces a pro-inflammatory Th1 immune response in a peroxidatic cysteine-dependent manner.Immunology · 2021Article
- DNA damage and oxidative stress in human cells infected by Trypanosoma cruzi.PLoS pathogens · 2021Article
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Modulation of the Host Nuclear Compartment byFrontiers in cellular and infection microbiology · 2021Article
- Article
- Drug transporter and oxidative stress gene expression in human macrophages infected with benznidazole-sensitive and naturally benznidazole-resistant Trypanosoma cruzi parasites treated with benznidazole.Parasites & vectors · 2019Article
- Host-parasite interaction: changes in human placental gene expression induced by Trypanosoma cruzi.Parasites & vectors · 2018Article
- Pathogenesis of Chronic Chagas Disease: Macrophages, Mitochondria, and Oxidative Stress.Current clinical microbiology reports · 2018Article
- EarlyFrontiers in microbiology · 2018Article
- Purinergic Antagonist Suramin Aggravates Myocarditis and Increases Mortality by Enhancing Parasitism, Inflammation, and Reactive Tissue Damage inOxidative medicine and cellular longevity · 2018Article
- Old Yellow Enzyme fromFrontiers in immunology · 2018Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma cruzi, the causative agent of Chagas disease, has the peculiarity, when compared with other intracellular parasites, that it is able to invade almost any type of cell. This property makes Chagas a complex parasitic disease in terms of prophylaxis and therapeutics. The identification of key host cellular factors that play a role in the T. cruzi invasion is important for the understanding of disease pathogenesis. In Chagas disease, most of the focus is on the response of macrophages and cardiomyocytes, since they are responsible for host defenses and cardiac lesions, respectively. In the present work, we studied the early response to infection of T. cruzi in human epithelial cells, which constitute the first barrier for establishment of infection. These studies identified up to 1700 significantly altered genes regulated by the immediate infection. The global analysis indicates that cells are literally reprogrammed by T. cruzi, which affects cellular stress responses (neutrophil chemotaxis, DNA damage response), a great number of transcription factors (including the majority of NF κ B family members), and host metabolism (cholesterol, fatty acids, and phospholipids). These results raise the possibility that early host cell reprogramming is exploited by the parasite to establish the initial infection and posterior systemic dissemination.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.