ArticleJournal of biomedicine & biotechnology2010
Mexican Trypanosoma cruzi T. cruzi I strains with different degrees of virulence induce diverse humoral and cellular immune responses in a murine experimental infection model.
Article in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
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- Chagas Disease in Pregnant Women from Endemic Regions Attending the Hospital General de Mexico, Mexico City.Tropical medicine and infectious disease · 2022Article
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- Characterisation of Macrophage Polarisation in Mice Infected with Ninoa Strain ofPathogens (Basel, Switzerland) · 2021Article
- Circulating miR-146a as a possible candidate biomarker in the indeterminate phase of Chagas disease.Biological research · 2021Article
- Electrolyzed Oxidizing Water Modulates the Immune Response in BALB/c Mice Experimentally Infected withPathogens (Basel, Switzerland) · 2020Article
- Repositioned Drugs for Chagas Disease Unveiled via Structure-Based Drug Repositioning.International journal of molecular sciences · 2020Article
- Differential gene expression of virulence factors modulates infectivity of TcI Trypanosoma cruzi strains.Parasitology research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is has been shown that the majority of T. cruzi strains isolated from Mexico belong to the T. cruzi I (TCI). The immune response produced in response to Mexican T. cruzi I strains has not been well characterized. In this study, two Mexican T. cruzi I strains were used to infect Balb/c mice. The Queretaro (TBAR/MX/0000/Queretaro)(Qro) strain resulted in 100% mortality. In contrast, no mortality was observed in mice infected with the Ninoa (MHOM/MX/1994/Ninoa) strain. Both strains produced extended lymphocyte infiltrates in cardiac tissue. Ninoa infection induced a diverse humoral response with a higher variety of immunoglobulin isotypes than were found in Qro-infected mice. Also, a stronger inflammatory TH1 response, represented by IL-12p40, IFNgamma, RANTES, MIG, MIP-1beta, and MCP-1 production was observed in Qro-infected mice when compared with Ninoa-infected mice. We propose that an exacerbated TH1 immune response is a likely cause of pathological damage observed in cardiac tissue and the primary cause of death in Qro-infected mice.
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