ArticleThe Journal of experimental medicine2007
Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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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.
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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.
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Who cites it
60 citing papers in PubMed, 106 citations in OpenAlex.
- Beyond cardiac embolism and cryptogenic stroke: unveiling the mechanisms of cerebrovascular events in Chagas disease.Lancet regional health. Americas · 2025Review
- Towards a map of the immune system manipulation network byFrontiers in cellular and infection microbiology · 2025Review
- Zileuton, a 5-Lypoxigenase Inhibitor, is Antiparasitic and Prevents Inflammation in the Chronic Stage of Heart Chagas Disease.ACS infectious diseases · 2024Article
- Article
- New Insights into the Role of thePathogens (Basel, Switzerland) · 2023Article
- Chagas Heart Disease: Beyond a Single Complication, from Asymptomatic Disease to Heart Failure.Journal of clinical medicine · 2022Review
- Disruption of multiple copies of the Prostaglandin F2alpha synthase gene affects oxidative stress response and infectivity in Trypanosoma cruzi.PLoS neglected tropical diseases · 2022Article
- Increased angiogenesis parallels cardiac tissue remodelling in experimental acute Trypanosoma cruzi infection.Memorias do Instituto Oswaldo Cruz · 2022Article
- Platelets, Macrophages, and Thromboinflammation in Chagas Disease.Journal of inflammation research · 2022Review
- Lipid droplets of protozoan parasites: survival and pathogenicity.Memorias do Instituto Oswaldo Cruz · 2022Article
- Complex and Controversial Roles of Eicosanoids in Fungal Pathogenesis.Journal of fungi (Basel, Switzerland) · 2021Review
- Resolvin D1 Administration Is Beneficial in Trypanosoma cruzi Infection.Infection and immunity · 2020Article
- The role of vascular endothelium and exosomes in human protozoan parasitic diseases.Vessel plus · 2020Article
- Co-opting oxylipin signals in microbial disease.Cellular microbiology · 2019Review
- Endothelins in inflammatory neurological diseases.Pharmacology & therapeutics · 2019Review
- A role for trypanosomatid aldo-keto reductases in methylglyoxal, prostaglandin and isoprostane metabolism.The Biochemical journal · 2018Article
- Infectious myocarditis: the role of the cardiac vasculature.Heart failure reviews · 2018Review
- Trypanosoma cruzi Produces the Specialized Proresolving Mediators Resolvin D1, Resolvin D5, and Resolvin E2.Infection and immunity · 2018Article
- Inflammatory and Pro-resolving Lipids in Trypanosomatid Infections: A Key to Understanding Parasite Control.Frontiers in microbiology · 2018Review
- Extracellular Vesicles Shed ByFrontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A(2) (TXA(2)). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA(2) is the predominant eicosanoid present in all life stages of T. cruzi. Parasite-derived TXA(2) accounts for up to 90% of the circulating levels of TXA(2) in infected wild-type mice, and perturbs host physiology. Mice in which the gene for the TXA(2) receptor (TP) has been deleted, exhibited higher mortality and more severe cardiac pathology and parasitism (fourfold) than WT mice after infection. Conversely, deletion of the TXA(2) synthase gene had no effect on survival or disease severity. TP expression on somatic cells, but not cells involved in either acquired or innate immunity, was the primary determinant of disease progression. The higher intracellular parasitism observed in TP-null ECs was ablated upon restoration of TP expression. We conclude that the host response to parasite-derived TXA(2) in T. cruzi infection is possibly an important determinant of mortality and parasitism. A deeper understanding of the role of TXA(2) may result in novel therapeutic targets for a disease with limited treatment options.
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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.