ArticleParasites & vectors2018
Host-parasite interaction: changes in human placental gene expression induced by Trypanosoma cruzi.
Article in Parasites & vectors, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Current approaches and developments in transcript profiling of the human placenta.Human reproduction update · 2020Pooled it
- Protein Kinase Inhibitors and Oxidative Stress Modulate In Vivo Phosphorylation ofPharmaceutics · 2026Article
- Placental transcriptome profiling in congenital Chagas disease: gene networks associated with transmission.Frontiers in cellular and infection microbiology · 2026Article
- Understanding Host-Pathogen Interactions in Congenital Chagas Disease Through Transcriptomic Approaches.Pathogens (Basel, Switzerland) · 2025Review
- In Vitro Identification of Phosphorylation Sites on TcPolβ by Protein Kinases TcCK1, TcCK2, TcAUK1, and TcPKC1 and Effect of Phorbol Ester on Activation by TcPKC of TcPolβ inMicroorganisms · 2024Article
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- New insights intoFrontiers in immunology · 2024Review
- Subunit nanovaccine elicited T cell functional activation controls Trypanosoma cruzi mediated maternal and placental tissue damage and improves pregnancy outcomes in mice.NPJ vaccines · 2023Article
- TORCH Congenital Syndrome Infections in Central America's Northern Triangle.Microorganisms · 2023Article
- The transcriptome landscape of 3D-cultured placental trophoblasts reveals activation of TLR2 and TLR3/7 in response to lowFrontiers in microbiology · 2023Article
- Animal Models ofPathogens (Basel, Switzerland) · 2022Review
- Kinetic Characterization and Inhibition ofBiochemistry · 2022Article
- MicroRNAs: master regulators in host-parasitic protist interactions.Open biology · 2022Review
- Ex Vivo Infection of Human Placental Explants byPathogens (Basel, Switzerland) · 2022Article
- Suprabasin-A Review.Genes · 2021Review
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Molecular dissection of Chagas induced cardiomyopathy reveals central disease associated and druggable signaling pathways.PLoS neglected tropical diseases · 2020Article
- 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
- Congenital Transmission ofFrontiers in microbiology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundChagas disease is caused by Trypanosoma cruzi, a parasite endemic to Latin America. Most infections occur in children by vector or congenital transmission. Trypanosoma cruzi establishes a complexity of specific molecular parasite-host cell interactions to invade the host. However, most studies have been mainly focused on the interaction between the parasite and different cell types, but not on the infection and invasion on a tissue level. During congenital transmission, T. cruzi must cross the placental barrier, composed of epithelial and connective tissues, in order to infect the developing fetus. Here we aimed to study the global changes of transcriptome in the placental tissue after a T. cruzi challenge.
resultsStrong changes in gene expression profiling were found in the different experimental conditions, involving the reprogramming of gene expression in genes involved in the innate immune response.
conclusionsTrypanosoma cruzi induces strong changes in genes involved in a wide range of pathways, especially those involved in immune response against infections.
Indexed as
Identifiers
What OpenQuestion holds
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.