Upregulation of cardiac IL-10 and downregulation of IFN- γ in Balb/c IL-4 −/− in acute chagasic myocarditis due to Colombian strain of Trypanosoma cruzi
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2018
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Inflammatory response in Chagas disease is related to parasite and host factors. However, immune system regulation has not been
fully elucidated. Thus, this study is aimed at evaluating IL-4 influence on acute phase of Trypanosoma cruzi experimental infection
through dosage of cytokine levels in cardiac homogenate of infected Balb/c WT and Balb/c IL-4−/− as well as its histopathological
repercussions. For such purpose, mice were divided into two groups: an infected group with 100 forms of the Colombian strain and
an uninfected group. After 21 days of infection, animals were euthanized and the blood, spleen, and heart were collected. The spleen
was used to culture splenic cells in 48 h. Subsequently, cytokines TNF-α, IL-12p70, IL-10, IFN-γ, and IL-17 were measured in the
blood, culture supernatant, and heart apex by ELISA. The base of the heart was used for histopathological analysis. From these
analysis, infected Balb/c IL-4−/− mice showed milder inflammatory infiltrate compared to Balb/c WT, but without changes in
nest density and collagen deposition. IL-4 absence culminated in lower cardiac tissue IFN-γ production, although it did not
affect TNF-α expression in situ. It also decreased TNF-α systemic production and increased IL-10, both systemically and in situ.
In addition, IL-4 absence did not influence IL-17 expression. Splenocytes of IL-4-deficient mice produced higher amounts of
IFN-γ, TNF-α, and IL-17 and lower amounts of IL-10. Thus, IL-4 absence in acute phase of experimental infection with T. cruzi
Colombian strain reduces myocarditis due to lower IFN-γ production and greater IL-10 production in situ and this pattern is
not influenced by splenocyte general repertoire.
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SILVA, Marcos Vinicius da et al. Upregulation of cardiac IL-10 and downregulation of IFN- γ in Balb/c IL-4 −/− in acute chagasic myocarditis due to Colombian strain of Trypanosoma cruzi. Mediators of Inflammation, Oxford, v. 2018, e3421897, 2018. DOI: 10.1155/2018/3421897. Disponível em: https://onlinelibrary.wiley.com/doi/10.1155/2018/3421897. Acesso em: 6 fev. 2025.