Thus, IL-4 absence in acute phase of experimental infection with <i>T. cruzi</i> Colombian strain reduces myocarditis due to lower IFN-<i>γ</i> production and greater IL-10 production <i>in situ</i> and this pattern is not influenced by splenocyte general repertoire.
After 20 days, infected mice presented reduced vitamin C and E tissue levels, high cytokines (interferon gamma, tumour necrosis factor-α, interleukin 10 and chemokine ligand 2), prostaglandin F2α (PGF2α ) and nitric oxide (NO) cardiac production, intense myocarditis and reactive tissue damage, which was directly correlated with the intensity of the inflammatory infiltrate and the degree of pathological cardiac remodelling.
Expression of miR-98 was higher, IL-10 was lower, in B cells isolated from the mouse hearts with myocarditis, which was negatively correlated with each other.
Only expression of IL-10 resulted in a highly significant decrease in myocardial inflammation and fibrosis, as well as an increased ejection fraction compared with controls.
On day 21, HE staining was performed to detect the myocardial inflammation and T lymphocyte proliferation assay was used to determine the effects of IL-10 gene transfected iDC on autoreactive T cell proliferation.