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Updated: Apr 14, 2026

Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
Published on: June 23, 2022
Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with
Bruna Perez Vazquez1, Thaís Perez Vazquez2, Camila Botelho Miguel3,4
1Disciplina de Biologia Celular/Instituto de Ciências Biológicas e Naturais, Universidade Federal do Triângulo Mineiro, Uberaba, 38061-500, Minas Gerais, Brazil. brunatpz@hotmail.com.
Insights
Higher parasite loads in Chagas disease lead to increased inflammation and intestinal damage. This study highlights the significant role of parasite burden in developing the digestive form of this neglected tropical disease.
Area of Science:
- Parasitology
- Immunology
- Gastroenterology
Background:
- Chagas disease, caused by Trypanosoma cruzi, affects cardiac, gastrointestinal, and nervous systems.
- The impact of parasite burden on Chagas disease inflammation and progression is not fully understood.
Purpose of the Study:
- To investigate the influence of Trypanosoma cruzi parasite load on intestinal lesions and inflammation in an acute experimental model.
- To assess correlations between parasite burden, inflammatory responses, and intestinal injury.
Main Methods:
- An acute experimental Chagas disease model in C57BL/6 mice was used.
- Mice were infected with low, medium, or high doses of Trypanosoma cruzi.
- Intestinal lesions, inflammation, and parasite load were evaluated at 7 and 14 days post-infection using various statistical analyses.
Main Results:
- High parasite loads resulted in faster and more severe parasitemia.
- Increased colon inflammation, myositis, periganglionitis, and pro-inflammatory cytokine levels (TNF-α, INF-γ, IL-2, IL-17, IL-6) were observed with higher parasite loads.
- A positive correlation was found between parasite load, inflammatory markers, and intestinal amastigote nests.
Conclusions:
- Experimental data indicate that parasite load significantly influences the intestinal inflammatory response in Trypanosoma cruzi infections.
- Parasite burden is a key factor contributing to the development of the digestive form of Chagas disease.
Background:
Chagas disease is caused by the protozoan Trypanosoma cruzi and is characterized by cardiac, gastrointestinal, and nervous system disorders. Although much about the pathophysiological process of Chagas disease is already known, the influence of the parasite burden on the inflammatory process and disease progression remains uncertain.
Methods:
We used an acute experimental disease model to evaluate the effect of T. cruzi on intestinal lesions and assessed correlations between parasite load and inflammation and intestinal injury at 7 and 14 days post-infection. Low (3 × 10(2)), medium (3 × 10(3)), and high (3 × 10(4)) parasite loads were generated by infecting C57BL/6 mice with "Y"-strain trypomastigotes. Statistical analysis was performed using analysis of variance with Tukey's multiple comparison post-test, Kruskal-Wallis test with Dunn's multiple comparison, χ2 test and Spearman correlation.
Results:
High parasite load-bearing mice more rapidly and strongly developed parasitemia. Increased colon width, inflammatory infiltration, myositis, periganglionitis, ganglionitis, pro-inflammatory cytokines (e.g., TNF-α, INF-γ, IL-2, IL-17, IL-6), and intestinal amastigote nests were more pronounced in high parasite load-bearing animals. These results were remarkable because a positive correlation was observed between parasite load, inflammatory infiltrate, amastigote nests, and investigated cytokines.
Conclusions:
These experimental data support the idea that the parasite load considerably influences the T. cruzi-induced intestinal inflammatory response and contributes to the development of the digestive form of the disease.
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