Alcohol exacerbates murine pulmonary tuberculosis
Alcohol exacerbates murine pulmonary tuberculosis
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DOI：
10.1128/iai.72.5.2556-2563.2004
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发表时间：
2004-05-01
影响因子：
3.1
通讯作者：
Nelson, S
中科院分区：
文献类型：
--
作者：
Mason, CM;Dobard, E;Nelson, S
饮酒被描述为结核分枝杆菌感染的一个危险因素，但它对结核病的贡献一直难以从其他不利的社会经济因素中分离出来。我们的目的是评估饮酒对肺部感染支原体的影响。结核病在小鼠模型中。BALB/c小鼠维持Lieber-DeCarli液体乙醇饮食或液体对照饮食，并用低剂量M.结核病H37 Rv.比较各组间的肺微生物负荷、肺和肺相关淋巴结CD 4（+）和CD 8（+）淋巴细胞数量和增殖率以及CD 4（+）淋巴细胞细胞因子产生水平。饮酒组小鼠肺内微生物负荷明显高于对照组，且小鼠肺部感染M.酒精组肺结核变钝。饮酒小鼠的CD 4（+）淋巴细胞的淋巴细胞增殖和γ干扰素的产生减少。此外，饮酒小鼠的肺肉芽肿明显较小。总之，小鼠饮酒与M.结核病，这是伴随着在区域特异性的CD 4（+）-和CD 8（+）-淋巴细胞反应和缺陷性肺肉芽肿形成的改变。
Alcohol consumption has been described as a risk factor for infection with Mycobacterium tuberculosis, but its contribution to tuberculosis has been difficult to isolate from other adverse socioeconomic factors. Our objective was to evaluate the impact of alcohol consumption on pulmonary infection with M. tuberculosis in a murine model. BALB/c mice were maintained on the Lieber-DeCarli liquid ethanol diet or a liquid control diet and infected intratracheally with low-dose M. tuberculosis H37Rv. Lung organism burdens, lung and lung-associated lymph node CD4(+)- and CD8(+)- lymphocyte numbers and rates of proliferation, and CD4(+)-lymphocyte cytokine production levels were compared between the groups. The alcohol-consuming mice had significantly higher lung organism burdens than the control mice, and the CD4(+)- and CD8(+)-lymphocyte responses to pulmonary infection with M. tuberculosis were blunted in the alcohol group. Lymphocyte proliferation and production of gamma interferon were decreased in the CD4(+) lymphocytes from the alcohol-consuming mice. Additionally, lung granulomas were significantly smaller in the alcohol-consuming mice. In conclusion, murine alcohol consumption is associated with decreased control of pulmonary infection with M. tuberculosis, which is accompanied by alterations in the region-specific CD4(+)- and CD8(+)-lymphocyte responses and defective lung granuloma formation.