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Alcohol Pre-Exposure in T. cruzi-Infected Mice Enhances IL-4 Production by CD8 T Cells and Modulates Innate Immunity
Paulo Henrique Tolentino Moura1, Beatriz Prado Noronha2, Marcio Sobreira Silva Araujo2
1Universidade Estadual de Montes Claros, UNIMONTES-PPGCS, Montes Claros, Minas Gerais, Brazil.
None:
Trypanosoma cruzi infection, which causes Chagas' disease, induces an immune response in the host whose efficiency is important for the infection to persist or be eliminated. Alcohol consumption produces a great impact on the immune system, inducing alterations in the determination of T lymphocyte effector function, directing the profile of these cells to tolerance or inflammation. Our study aimed to evaluate, in C57BL/6 mice, the cytokine production in splenic leukocytes from T. cruzi infected and treated (EtOH) for 15 days and controls. Twenty-four mice were randomised into four groups, with 12 animals each: (1) Non-Infected Control (NI), (2) Control Infected (CI), (3) Experimental Non-Infected (EtOH-NI), and (4) Experimental Infected (EtOH-I). Ethanol-pre-exposed infected mice exhibited elevated parasitaemia during the patent period compared to controls. Adaptive immunity was characterised by increased IL-4, IL-10 and IFN-γ production by CD8+ T lymphocytes, while innate immunity showed reduced cytokine production, particularly in NK cells and macrophages. Ethanol amplified IL-10 and IFN-γ responses in macrophages yet suppressed TNF-α production in dendritic cells and macrophages during infection. These findings suggest ethanol modulates the immune response by enhancing adaptive immunity while impairing innate mechanisms, contributing to altered host-pathogen dynamics in T. cruzi infection.

