ArticleInternational journal of experimental pathology2002
Evidence for a perforin-mediated mechanism controlling cardiac inflammation in Trypanosoma cruzi infection.
Article in International journal of experimental pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 35 citations in OpenAlex.
- Kinetics of Biomarkers for Therapeutic Assessment in Swiss Mice Infected with a VirulentPathogens (Basel, Switzerland) · 2026Article
- In the Acute Phase ofFrontiers in immunology · 2022Article
- Rapamycin Treatment Reduces Acute Myocarditis Induced by Trypanosoma cruzi Infection.Journal of innate immunity · 2020Article
- Role of Inactive and ActiveFrontiers in microbiology · 2017Article
- Immunoregulatory mechanisms in Chagas disease: modulation of apoptosis in T-cell mediated immune responses.BMC infectious diseases · 2016Article
- Mast cell function and death in Trypanosoma cruzi infection.The American journal of pathology · 2011Article
- Specific antibodies induce apoptosis in Trypanosoma cruzi epimastigotes.Parasitology research · 2010Article
- Perforin-expressing cytotoxic cells contribute to chronic cardiomyopathy in Trypanosoma cruzi infection.International journal of experimental pathology · 2010Article
- Fas ligand-dependent inflammatory regulation in acute myocarditis induced by Trypanosoma cruzi infection.The American journal of pathology · 2007Article
- Distinct kinetics of effector CD8+ cytotoxic T cells after infection with Trypanosoma cruzi in naive or vaccinated mice.Infection and immunity · 2006Article
- Experimental infection with Trypanosoma cruzi increases the population of CD8(+), but not CD4(+), immunoglobulin G Fc receptor-positive T lymphocytes.Infection and immunity · 2005Article
- Selenium supplementation at low doses contributes to the decrease in heart damage in experimental Trypanosoma cruzi infection.Parasitology research · 2003Article
- Benznidazole treatment following acute Trypanosoma cruzi infection triggers CD8+ T-cell expansion and promotes resistance to reinfection.Antimicrobial agents and chemotherapy · 2002Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD8+ T lymphocytes are considered an important cell population involved in the control of parasitaemia and mortality after Trypanosoma cruzi infection. However, despite recent developments in this field, the mechanism whereby this control is exerted is still not completely understood. Here we have used perforin knockout (-/-) mice infected with Y strain T. cruzi in order to evaluate specifically the participation of the perforin-based cytotoxic pathway in the destruction of cardiomyocytes, cellular inflammatory infiltration, and control of parasitaemia and mortality. We observed that although parasitaemia was equivalent in perforin (+/+) and (-/-) groups, survival rate and spontaneous physical performance were significantly lower in the perforin deficient mice. The cardiac inflammatory cell infiltration, mostly composed of CD8+ cells, was more evident in perforin (-/-) mice. Ultrastructural and immunofluorescence analysis, as well as plasma creatine kinase activity, revealed cardiomyocyte damage and necrosis, more evident in perforin (-/-) mice. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) assays performed in heart samples revealed similar and modest levels of apoptosis in both perforin (+/+) and (-/-) mice. These results indicate that perforin does not play a pivotal role in the control of parasitaemia and direct lysis of cardiomyocytes, but seems to be an important molecule involved in the control of cardiac inflammation and pathology induced by a highly virulent strain of T. cruzi.
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