ArticleMemorias do Instituto Oswaldo Cruz2015
Role of cyclooxygenase-2 in Trypanosoma cruzi survival in the early stages of parasite host-cell interaction.
Article in Memorias do Instituto Oswaldo Cruz, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- The roles of COX-2 in protozoan infection.Frontiers in immunology · 2023Review
- Motility patterns of Trypanosoma cruzi trypomastigotes correlate with the efficiency of parasite invasion in vitro.Scientific reports · 2020Article
- Amlodipine Increases the Therapeutic Potential of Ravuconazole upon Trypanosoma cruzi Infection.Antimicrobial agents and chemotherapy · 2020Article
- Cyclooxygenase (COX)-2 Inhibitors ReduceFrontiers in microbiology · 2019Article
- Differential expression of proteins in genetically distinct Trypanosoma cruzi samples (TcI and TcII DTUs) isolated from chronic Chagas disease cardiac patients.Parasites & vectors · 2018Article
- Outcome of E1224-Benznidazole Combination Treatment for Infection with a Multidrug-Resistant Trypanosoma cruzi Strain in Mice.Antimicrobial agents and chemotherapy · 2018Article
- Extracellular Vesicles Shed ByFrontiers in immunology · 2018Article
- Protective effect of aspirin treatment on mouse behavior in the acute phase of experimental infection with Trypanosoma cruzi.Parasitology research · 2018Article
- Implication of Apoptosis for the Pathogenesis ofFrontiers in immunology · 2017Review
- Response toFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chagas disease, caused by the intracellular protozoan Trypanosoma cruzi, is a serious health problem in Latin America. During this parasitic infection, the heart is one of the major organs affected. The pathogenesis of tissue remodelling, particularly regarding cardiomyocyte behaviour after parasite infection and the molecular mechanisms that occur immediately following parasite entry into host cells are not yet completely understood. When cells are infected with T. cruzi, they develop an inflammatory response, in which cyclooxygenase-2 (COX-2) catalyses rate-limiting steps in the arachidonic acid pathway. However, how the parasite interaction modulates COX-2 activity is poorly understood. In this study, the H9c2 cell line was used as our model and we investigated cellular and biochemical aspects during the initial 48 h of parasitic infection. Oscillatory activity of COX-2 was observed, which correlated with the control of the pro-inflammatory environment in infected cells. Interestingly, subcellular trafficking was also verified, correlated with the control of Cox-2 mRNA or the activated COX-2 protein in cells, which is directly connected with the assemble of stress granules structures. Our collective findings suggest that in the very early stage of the T. cruzi-host cell interaction, the parasite is able to modulate the cellular metabolism in order to survives.
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