Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus.
Alcohol consumption during murine acquired immunodeficiency syndrome accentuates heart pathology due to coxsackievirus.
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小鼠获得性免疫缺陷综合征期间的饮酒会加重柯萨奇病毒引起的心脏病。
DOI：
10.1093/alcalc/37.2.157
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Watson,RonaldR
中科院分区：
文献类型：
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作者：
Sepúlveda,RTomás;Jiang,Shuguang;Besselsen,DavidG;Watson,RonaldR
酒精，尤其是长期过量饮酒后，会导致宿主免疫力显着改变，并增加感染的可能性。为了确定小鼠获得性免疫缺陷综合征 (AIDS) 期间乙醇消耗是否会加剧柯萨奇病毒 B3 心肌病，雌性 C57BL/6 小鼠感染 LP-BM5 逆转录病毒，并给予 40% 乙醇水溶液和固体琼脂形式的小鼠。半定量评估心脏组织病理学的病变严重程度和诱导的脾细胞产生：测定白细胞介素（IL）-2、IL-4、IL-6、肿瘤坏死因子-α和干扰素-γ。小鼠逆转录病毒感染期间的乙醇消耗增加了 85% 的动物柯萨奇病毒诱发的心肌炎，并加剧了病变的严重程度。感染逆转录病毒和同时感染柯萨奇病毒的小鼠表现出明显的心脏病变。逆转录病毒感染抑制 Th1 反应，导致细胞因子失调和免疫抑制，从而促进柯萨奇病毒诱发的心肌炎。我们的数据表明，乙醇消耗会加剧细胞因子失衡，通过增强 Th2 和/或抑制 Th1 功能来促进 Th2 反应。总之，小鼠艾滋病在柯萨奇病毒感染期间促进了严重的心脏毒性，而未感染逆转录病毒的小鼠则具有抵抗力。乙醇的消耗加剧了这些影响。
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-α and interferon-γ 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.