Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus.

摘要

Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40 ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-alpha and interferon-gamma were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85 of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.