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Response to Infection by Trypanosoma cruzi in a Murine Model
Mariana De Alba-Alvarado1, Martha Irene Bucio-Torres1, Edgar Zenteno2
1Departamento de Microbiología y Parasitología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Insights
This study in mice reveals Chagas disease progression, defining the acute phase from 1-60 days post-infection and the chronic phase starting at 62 days. Fibrotic damage, a hallmark of Chagas disease cardiopathy, results from sustained inflammation.
Area of Science:
- * Parasitology and Immunology
- * Pathology and Disease Mechanisms
Background:
- * Chagas disease cardiomyopathy is an irreversible complication of chronic infection.
- * The precise definition and progression from acute to chronic Chagas disease remain debated.
- * Understanding disease progression is crucial for developing effective interventions.
Purpose of the Study:
- * To correlate parasite presence with cardiac tissue changes and disease progression in a murine model.
- * To define the temporal dynamics of acute and chronic phases of Chagas disease.
- * To investigate the relationship between parasitemia, inflammation, fibrosis, and seropositivity.
Main Methods:
- * Infection of CD1 mice with *Trypanosoma cruzi* and saline controls.
- * Quantification of parasitemia and IgG titers via ELISA.
- * Histological analysis of cardiac tissues (HE and Masson trichrome staining) at various time points.
Main Results:
- * Significant parasitemia observed from 15 days post-infection (dpi), peaking at 33 dpi.
- * Amastigote nests detected from 15-62 dpi; lymphocytic infiltration and fibrosis present from 8 dpi to 100 dpi.
- * Chronic phase, marked by absence of amastigotes and presence of inflammation/fibrosis, initiated at 62 dpi.
Conclusions:
- * The murine model effectively replicates acute and chronic Chagas disease phases.
- * The acute phase spans 1-60 dpi, with the chronic phase beginning at 62 dpi.
- * Fibrotic damage in Chagas disease cardiopathy is a consequence of persistent inflammatory infiltration, initiating in the acute phase.
Abstract:
Cardiopathy is a common, irreversible manifestation of the chronic phase of Chagas disease; however, there is controversy as to how the causes for progression from the acute to the chronic phase are defined. In this work, the presence of the parasite is correlated with the occurrence of cell infiltration and fibrosis in cardiac tissues, as well as IgG detection and disease progression in a murine model. Fifty CD1 mice were infected intraperitoneally with Trypanosoma cruzi, while 30 control were administered with saline solution. Parasitemia levels were determined, and IgG titers were quantified by ELISA. At different times, randomly selected mice were euthanized, and the heart was recovered. Cardiac tissue slides were stained with HE and Masson trichrome stain. A significant increase in parasitemia levels was observed after 15 days post-infection (dpi), with a maximum of 4.1 × 106 parasites on 33 dpi, ending on 43 dpi; amastigote nests were observed on 15-62 dpi. Histological analysis revealed lymphocytic infiltration and fibrotic lesions from 8 dpi until the end of the study, on 100 dpi. The presence of plasma cells in the myocardium observed on 40-60 dpi, accompanied by seropositivity to ELISA on 40-100 dpi, was regarded as the hallmark of the transition phase. Meanwhile, the chronic phase, characterized by the absence of amastigotes, presence of cell infiltration, fibrotic lesions, and seropositivity, started on 62 dpi. A strong correlation between parasitemia and the presence of amastigote nests was found (r 2 = 0.930), while correlation between the presence of fibrosis and of amastigote nests was weak (r 2 = 0.306), and that between fibrosis and lymphocyte infiltration on 100 dpi was strong (r 2 = 0.899). The murine model is suitable to study Chagas disease, since it can reproduce the chronic and acute phases of the human disease. The acute phase was determined to occur on 1-60 dpi, while the chronic phase starts on 62 dpi, and fibrotic damage is a consequence of the continuous inflammatory infiltration; on the other hand, fibrosis was determined to start on the acute phase, being more apparent in the chronic phase, when Chagas disease-related cardiopathy is induced.
