ArticleMedical microbiology and immunology2012
Toll-like receptor-2 and interleukin-6 mediate cardiomyocyte protection from apoptosis during Trypanosoma cruzi murine infection.
Article in Medical microbiology and immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- CD73 activity controls cytotoxic CD4 T-cell response driving myocardial pathology in chronic Chagas disease.Frontiers in immunology · 2026Article
- Purinergic signaling modulates CD4+ T cells with cytotoxic potential during Trypanosoma cruzi infection.The Journal of clinical investigation · 2025Article
- Exercise training reduces cardiac fibrosis, promoting improvement in arrhythmias and cardiac dysfunction in an experimental model of chronic chagasic cardiomyopathy.Frontiers in physiology · 2025Article
- Exercise training combined with alprostadil improves myocardial infarction and coronary microcirculation disorder in aged rats by inhibiting mitogen-activated protein kinase (MAPK) signaling pathway activation.Annals of translational medicine · 2022Article
- Article
- The expression of TLR2 and TLR4 in the kidneys and heart of mice infected with Acanthamoeba spp.Parasites & vectors · 2020Article
- Article
- Identification of Candidate Signature Genes and Key Regulators Associated With Trypanotolerance in the Sheko Breed.Frontiers in genetics · 2019Article
- Interleukin-6 signalling mediates Galectin-8 co-stimulatory activity of antigen-specific CD4 T-cell response.Immunology · 2018Article
- MyD88 activation in cardiomyocytes contributes to the heart immune response to acute Trypanosoma cruzi infection with no effect on local parasite control.PLoS neglected tropical diseases · 2018Article
- Atrial Fibrillation Promotion in a Rat Model of Rheumatoid Arthritis.Journal of the American Heart Association · 2017Article
- New Insights into the Immunobiology of Mononuclear Phagocytic Cells and Their Relevance to the Pathogenesis of Cardiovascular Diseases.Frontiers in immunology · 2017Review
- Trypanosoma cruzi infection induces the expression of CD40 in murine cardiomyocytes favoring CD40 ligation-dependent production of cardiopathogenic IL-6.Parasitology research · 2016Article
- IL-6 Improves the Nitric Oxide-Induced Cytotoxic CD8+ T Cell Dysfunction in Human Chagas Disease.Frontiers in immunology · 2016Article
- Innate immunity and cardiomyocytes in ischemic heart disease.Life sciences · 2014Review
- Trypanosoma cruzi parasites fight for control of the JAK-STAT pathway by disarming their host.JAK-STAT · 2014Review
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Local innate immunity plays a key role in initiating and coordinating homeostatic and defense responses in the heart. We have previously reported that the cardiotropic parasite Trypanosoma cruzi, the etiological agent of Chagas disease, protects cardiomyocytes against growth factor deprivation-induced apoptosis. In this study, we investigated cardiomyocyte innate immune response to T. cruzi infection and its role in cellular protection from apoptosis. We found that Toll-like receptor (TLR) 2-expressing cells were strongly increased by the parasite in BALB/c neonatal mouse cardiomyocyte cultures. Using a dominant-negative system, we showed that TLR2 mediated cardiomyocyte survival and the secretion of interleukin (IL) 6, which acted as an essential anti-apoptotic factor. Moreover, IL6 released by infected cells, as well as the recombinant bioactive cytokine, induced the phosphorylation of the signal transducers and activators of transcription-3 (STAT3) in cultured cardiomyocytes. In accord with the in vitro results, during the acute phase of the infection, TLR2 expression increased 2.9-fold and the anti-apoptotic factor Bcl-2 increased 4.5-fold in the cardiac tissue. We have clearly shown a cross-talk between the intrinsic innate response of cardiomyocytes and the pro-survival effect evoked by the parasite.
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