ABSTRACT 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.
Moura et al. (Fri,) studied this question.