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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.

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load