ArticlePLoS neglected tropical diseases2015
Cyclooxygenase-2 and Prostaglandin E2 Signaling through Prostaglandin Receptor EP-2 Favor the Development of Myocarditis during Acute Trypanosoma cruzi Infection.
Article in PLoS neglected tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 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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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Functional genomics of trypanotolerant and trypanosusceptible cattle infected with Trypanosoma congolense across multiple time points and tissues.PLoS neglected tropical diseases · 2025Article
- Toll-like receptors ligand immunomodulators for the treatment congenital diaphragmatic hernia.Orphanet journal of rare diseases · 2024Article
- Immunomodulatory proteins from hookworms reduce cardiac inflammation and modulate regulatory responses in a mouse model of chronicFrontiers in parasitology · 2023Article
- Interleukin-9 in Immunopathology ofFrontiers in cellular and infection microbiology · 2021Article
- Myeloid-Derived Suppressor Cells inFrontiers in cellular and infection microbiology · 2021Review
- Review
- Interaction of Signaling Lymphocytic Activation Molecule Family 1 (SLAMF1) receptor with Trypanosoma cruzi is strain-dependent and affects NADPH oxidase expression and activity.PLoS neglected tropical diseases · 2020Article
- Differences in cNOS/iNOS Activity during Resistance to Trypanosoma cruzi Infection in 5-Lipoxygenase Knockout Mice.Mediators of inflammation · 2019Article
- Cyclooxygenase (COX)-2 Inhibitors ReduceFrontiers in microbiology · 2019Article
- Curcumin exerts anti-inflammatory and vasoprotective effects through amelioration of NFAT-dependent endothelin-1 production in mice with acute Chagas cardiomyopathy.Memorias do Instituto Oswaldo Cruz · 2018Article
- Inflammatory and Pro-resolving Lipids in Trypanosomatid Infections: A Key to Understanding Parasite Control.Frontiers in microbiology · 2018Review
- Regulatory Lymphoid and Myeloid Cells Determine the Cardiac Immunopathogenesis ofFrontiers in microbiology · 2018Review
- L-arginine supplementation reduces mortality and improves disease outcome in mice infected with Trypanosoma cruzi.PLoS neglected tropical diseases · 2018Article
- Response toFrontiers in microbiology · 2017Article
- Correction: Cyclooxygenase-2 and Prostaglandin E2 Signaling through Prostaglandin Receptor EP-2 Favor the Development of Myocarditis during Acute Trypanosoma cruzi Infection.PLoS neglected tropical diseases · 2015Article
- Doxycycline and Benznidazole Reduce the Profile of Th1, Th2, and Th17 Chemokines and Chemokine Receptors in Cardiac Tissue from ChronicMediators of inflammationArticle
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Prostanoids are regulators of homeostasis and inflammation and are produced mainly by myeloid cells, being cyclooxygenases, COX-1 and COX-2, the key enzymes in their biosynthesis from arachidonic acid (AA). Here, we have investigated the expression of enzymes involved in AA metabolism during T. cruzi infection. Our results show an increase in the expression of several of these enzymes in acute T. cruzi infected heart. Interestingly, COX-2 was expressed by CD68+ myeloid heart-infiltrating cells. In addition, infiltrating myeloid CD11b+Ly6G- cells purified from infected heart tissue express COX-2 and produce prostaglandin E2 (PGE2) ex vivo. T. cruzi infections in COX-2 or PGE2-dependent prostaglandin receptor EP-2 deficient mice indicate that both, COX-2 and EP-2 signaling contribute significantly to the heart leukocyte infiltration and to the release of chemokines and inflammatory cytokines in the heart of T. cruzi infected mice. In conclusion, COX-2 plays a detrimental role in acute Chagas disease myocarditis and points to COX-2 as a potential target for immune intervention.
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Registered trials
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