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<p>Chagas disease (CD), caused by <i>Trypanosoma cruzi</i>, leads to cardiomyopathy in approximately 20–30% of infected individuals. Interleukin-11 (IL-11) has been implicated in cardiac fibrosis, although its immunological role in this context remains unclear. This study investigated the temporal dynamics of IL-11 and its receptor, IL-11Rα, expression in the hearts of C57BL/6 mice infected with 1,000 trypomastigote forms of the Y or Colombian strains of <i>T. cruzi</i>. Mice were euthanized at 5, 15, 30, 60, and 120&#xa0;days post-infection (dpi). Survival, parasitemia, and body and heart weights were monitored. Cardiac tissue was analyzed for parasite nests, myocarditis, collagen deposition, and expression of the IL-11 receptor alpha (IL-11Rα). Cytokine profiles were evaluated by ELISA and Cytometric Bead Array. Histopathological analysis revealed more intense myocarditis, parasite load, and collagen deposition in mice infected with the Colombian strain. Both strains induced IFN-γ, TNF-α, and IL-6 in cardiac tissue; however, IL-10, IL-4, and IL-17 were detected only in the Y strain, indicating a more balanced immune response. Despite the absence of significant IL-11 upregulation in either infection, IL-11Rα expression was progressively increased over time and positively correlated with collagen deposition. These findings suggest that IL-11Rα may play a role in cardiac remodeling and fibrosis independently of IL-11 upregulation. The results reinforce the importance of <i>T. cruzi </i>strain variability in disease outcome and highlight the IL-11/IL-11Rα axis as a potential target for further investigation in Chagas cardiomyopathy.</p> Graphical Abstract <p>The kinetics of IL-11 and IL-11Rα expression in the heart during experimental <i>Trypanosoma cruzi</i> infection reveal striking differences between the Y and Colombian strains over time (5, 15, 30, 60, and 120&#xa0;days post-infection). The shaded areas in green and orange represent IL-11Rα expression and IL-11 production, respectively. In the Y strain, IL-11 production is detectable throughout the infection, peaking around 30&#xa0;days. In contrast, the Colombian strain exhibits lower IL-11 expression. IL-11Rα expression is upregulated in both strains: starting at 15 dpi in the Y strain and at 60 dpi in the Colombian strain, remaining elevated until 120 dpi. The colored lines indicate the kinetics of other parameters: Pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6): red; Regulatory/Th2/Th17 cytokines (IL-10, IL-4, IL-17): green; Cardiac parasitism (<i>T. cruzi</i> nests): purple; Inflammatory infiltrate: black; Collagen deposition: brown. The distinct peaks observed between groups reflect the specific immunopathological characteristics of each strain in terms of inflammation, immune response, and cardiac damage. This graphic scheme provides an integrated summary of the dynamics between the analyzed parameters throughout the course of infection.</p> <p></p>

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Evaluation of Cardiac IL-11 and IL-11Rα Expression During T. cruzi Infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月12日

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  • Yarlla Loyane Lira Braga,
  • José Rodrigues do Carmo Neto,
  • Pablo Igor Ribeiro Franco,
  • Jordana Fernandes de Oliveira,
  • Rafael Obata Trevisan,
  • Fernanda Bernadelli de Vito,
  • Flávia Aparecida de Oliveira,
  • Mara Rúbia Nunes Celes,
  • Marcos Vinícius da Silva,
  • Juliana Reis Machado

摘要

Chagas disease (CD), caused by Trypanosoma cruzi, leads to cardiomyopathy in approximately 20–30% of infected individuals. Interleukin-11 (IL-11) has been implicated in cardiac fibrosis, although its immunological role in this context remains unclear. This study investigated the temporal dynamics of IL-11 and its receptor, IL-11Rα, expression in the hearts of C57BL/6 mice infected with 1,000 trypomastigote forms of the Y or Colombian strains of T. cruzi. Mice were euthanized at 5, 15, 30, 60, and 120 days post-infection (dpi). Survival, parasitemia, and body and heart weights were monitored. Cardiac tissue was analyzed for parasite nests, myocarditis, collagen deposition, and expression of the IL-11 receptor alpha (IL-11Rα). Cytokine profiles were evaluated by ELISA and Cytometric Bead Array. Histopathological analysis revealed more intense myocarditis, parasite load, and collagen deposition in mice infected with the Colombian strain. Both strains induced IFN-γ, TNF-α, and IL-6 in cardiac tissue; however, IL-10, IL-4, and IL-17 were detected only in the Y strain, indicating a more balanced immune response. Despite the absence of significant IL-11 upregulation in either infection, IL-11Rα expression was progressively increased over time and positively correlated with collagen deposition. These findings suggest that IL-11Rα may play a role in cardiac remodeling and fibrosis independently of IL-11 upregulation. The results reinforce the importance of T. cruzi strain variability in disease outcome and highlight the IL-11/IL-11Rα axis as a potential target for further investigation in Chagas cardiomyopathy.

Graphical Abstract

The kinetics of IL-11 and IL-11Rα expression in the heart during experimental Trypanosoma cruzi infection reveal striking differences between the Y and Colombian strains over time (5, 15, 30, 60, and 120 days post-infection). The shaded areas in green and orange represent IL-11Rα expression and IL-11 production, respectively. In the Y strain, IL-11 production is detectable throughout the infection, peaking around 30 days. In contrast, the Colombian strain exhibits lower IL-11 expression. IL-11Rα expression is upregulated in both strains: starting at 15 dpi in the Y strain and at 60 dpi in the Colombian strain, remaining elevated until 120 dpi. The colored lines indicate the kinetics of other parameters: Pro-inflammatory cytokines (TNF-α, IFN-γ, IL-6): red; Regulatory/Th2/Th17 cytokines (IL-10, IL-4, IL-17): green; Cardiac parasitism (T. cruzi nests): purple; Inflammatory infiltrate: black; Collagen deposition: brown. The distinct peaks observed between groups reflect the specific immunopathological characteristics of each strain in terms of inflammation, immune response, and cardiac damage. This graphic scheme provides an integrated summary of the dynamics between the analyzed parameters throughout the course of infection.