Chagas disease, caused by Trypanosoma cruzi, can show a variety of clinical outcomes ranging from mild symptoms to Chagas cardiomyopathy, the most severe and life-threatening manifestation of the disease. The degree of virulence is influenced by both parasite and host factors. In this study, we characterized a murine infection model using the T. cruzi Dm28c strain in BALB/c mice to assess disease progression. Infected mice showed a peak of parasitemia at 14 dpi, followed by a progressive decrease. Spleen weight increased up to sixfold compared to uninfected controls at 14 and 21 dpi, correlating with parasitemia levels. Histological analysis revealed focal inflammatory infiltrates in the heart starting at 7 dpi, with maximal intensity at 14 and 21 dpi. The expression of inflammatory cytokines (IFN-γ, IL-1β, TNF-α) and anti-inflammatory cytokines (IL-10, TGF-β) in the spleen showed a dynamic profile, with an early increase during the acute phase. The Dm28c infection of BALB/c mice can be considered as a non-lethal Chagas disease experimental model, with detectable parasitemia during the acute phase and a controlled inflammatory response.