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Interleukin-32γ in the Control of Acute Experimental Chagas Disease
Yarlla L L Braga1, José R C Neto1, Arthur W F Costa1
1Instituto de Patologia Tropical e Saúde Pública, Universidade Federal de Goiás, Goiânia, GO, Brazil.
Insights
Interleukin-32 gamma (IL-32γ) improved control of Chagas disease (CD) in mice. This immune response led to reduced parasite load and better survival during the acute phase of infection.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Chagas disease (CD), caused by *Trypanosoma cruzi*, is a significant parasitic illness.
- Interleukin-32 (IL-32) is implicated in inflammatory and adaptive immune responses (Th1/Th17).
Purpose of the Study:
- To investigate the role of Interleukin-32 gamma (IL-32γ) in the immune response, myocarditis pathogenesis, and disease control during acute experimental Chagas disease.
- To assess the impact of human IL-32γ expression on *T. cruzi* infection in a mouse model.
Main Methods:
- C57BL/6 wild-type (WT) and IL-32γ transgenic (IL-32γTg) mice were infected with *T. cruzi* (Colombian strain).
- Cardiac tissues were analyzed histopathologically for parasite nests, myocarditis, and collagen.
- Cytokine levels (IL-32, IFN-γ, TNF-α, IL-10, IL-17) in cardiac homogenates were quantified using ELISA.
Main Results:
- IL-32γTg mice exhibited superior control of parasitemia and fewer *T. cruzi* nests in the heart compared to WT mice.
- While IFN-γ, TNF-α, and IL-17 levels were similar, IL-10 expression was significantly higher in IL-32γTg mice.
- The observed cytokine profile in IL-32γTg mice correlated with better body weight maintenance, parasitemia control, and increased survival.
Conclusions:
- Human IL-32γ expression significantly contributes to controlling *T. cruzi* infection during the acute phase of Chagas disease in mice.
- The enhanced immune response, particularly elevated IL-10, in IL-32γTg mice plays a crucial role in mitigating disease severity.
Abstract:
Chagas disease (CD) is an important parasitic disease caused by Trypanosoma cruzi. Interleukin-32 (IL-32) plays an important role in inflammation and in the development of Th1/Th17 acquired immune responses. We evaluated the influence of IL-32γ on the immune response profile, pathogenesis of myocarditis in acute experimental CD, and control of the disease. For this, C57BL/6 wild-type (WT) and IL-32γTg mice were infected subcutaneously with 1,000 forms of Colombian strain of T. cruzi. In the histopathological analyzes, T. cruzi nests, myocarditis, and collagen were quantified in cardiac tissue. Cytokine productions (IL-32, IFN-γ, TNF-α, IL-10, and IL-17) were measured in cardiac homogenate by ELISA. The IL-32γTg mice showed a better control of parasitemia and T. cruzi nests in the heart than WT mice. Infected-WT and -IL-32γTg mice showed similar levels of IFN-γ, TNF-α, and IL-17, but IL-10 was significantly higher expressed in IL-32γTg than in WT mice. The cytokine profile found in IL-32γTg animals contributed to body weight maintenance, parasitemia control, and survival. Our results indicate that the presence of human IL-32γ in mice infected with the Colombian strain of T. cruzi is important for infection control during the acute phase of Chagas disease.
