Side-stream cigarette smoke accentuates immunomodulation during murine AIDS.

Side-stream cigarette smoke accentuates immunomodulation during murine AIDS.
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侧流香烟烟雾会增强小鼠艾滋病期间的免疫调节作用。

DOI:
10.1016/s1567-5769(02)00012-7
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发表时间:
2002
影响因子:
5.6
通讯作者:
Watson,RonaldRoss
Watson,RonaldRoss
中科院分区:
医学2区
文献类型:
--
作者:
Zhang,Jin;DuEster,En-Jie;Watson,RonaldRoss

文献摘要

被引文献

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对于不吸烟的人来说,侧流香烟的烟雾已经成为社会、政治和科学上一个备受争议的健康和安全问题。侧流香烟烟雾对人体健康的有害影响是它对免疫系统的不利影响,特别是在已经受到其他因素损害的情况下。获得性免疫缺陷综合征(AIDS)是由人类免疫缺陷病毒(HIV)引起的一种临床疾病。为了便于研究,我们利用模拟人类艾滋病的LP-BM5小鼠白血病病毒感染C57BL/6小鼠诱导小鼠艾滋病。逆转录病毒感染2周后,小鼠使用侧流香烟烟雾暴露系统暴露在侧流香烟烟雾中30分钟,每周5天,持续12周。小鼠逆转录病毒感染降低了魔豆蛋白A刺激的T淋巴细胞体外增殖,增加了促炎细胞因子白细胞介素-6 (IL-6)和肿瘤坏死因子-α (TNF-α)的释放,增加了肝脏脂质过氧化,降低了肝脏、肺和心脏α-生育酚水平。同时暴露于侧流香烟烟雾12周,进一步抑制逆转录病毒感染小鼠的T细胞增殖,增加TNF-α、IL-6细胞因子的释放,并增强肝脂质过氧化。在逆转录病毒感染期间,暴露于侧流香烟烟雾也会进一步增加α-生育酚的损失。我们的结论是,侧流香烟烟雾引起氧化应激增加、营养物质浓度降低和免疫功能抑制,可能使患有小鼠艾滋病的小鼠更容易受到机会性感染,可能加速小鼠艾滋病的进展。因此,减少侧流烟气暴露是提高艾滋病患者生活质量和数量的重要健康问题。
Side-stream cigarette smoke has become a hotly debated social, political, and scientific health and safety issue for nonsmokers. The harmful influences of side-stream cigarette smoke on human health are its adverse effects on the immune system, especially when already compromised by other agents. Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by human immunodeficiency virus (HIV). To facilitate studies, murine AIDS was induced in C57BL/6 mice by LP-BM5 murine leukemia virus infection, which mimics human AIDS. After 2 weeks of retroviral infection, the mice were exposed to side-stream cigarette smoke for 30 min, 5 days/week for 12 weeks using a side-stream cigarette smoke exposure system. Murine retrovirus infection reduced the in vitro proliferation of T lymphocytes stimulated by concanavalin A, increased the release of pro-inflammatory cytokine interleukin-6 (IL-6) tumor necrosis factor-alpha (TNF-α), increased the hepatic lipid peroxidation and decreased the α-tocopherol levels in liver, lung and heart. Concomitant side-stream cigarette smoke exposure for 12 weeks further inhibited the proliferation of T cells, increased the release of TNF-α, IL-6 cytokines and enhanced the hepatic lipid peroxidation from retrovirus infected mice. The loss of α-tocopherol was also further enhanced by side-stream cigarette smoke exposure during retrovirus infection. Our conclusions are that side-stream cigarette smoke induced increasing oxidative stress, reducing nutrient concentrations and suppressing immune function could make mice with murine AIDS more susceptible to opportunistic infections, potentially accelerating murine AIDS progression. Thus, the reduction of side-stream cigarette smoke exposure is an important health issue in AIDS patients to improve the quality and quantity of their lives.