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首页> 外文期刊>American Journal of Physiology >HIV-1-induced pulmonary oxidative and nitrosative stress: exacerbated response to endotoxin administration in HIV-1 transgenic mouse model.
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HIV-1-induced pulmonary oxidative and nitrosative stress: exacerbated response to endotoxin administration in HIV-1 transgenic mouse model.

机译：HIV-1诱导的肺部氧化和亚硝化应激：在HIV-1转基因小鼠模型中对内毒素给药的反应加剧。

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Human immunodeficiency virus (HIV)-1 causes lung disease by increasing the host's susceptibility to pathogens. HIV-1 also causes an increase in systemic oxidativeitrosative stress, perhaps enhancing the deleterious effects of secondary infections. Here we examined the ability of HIV-1 proteins to increase lung oxidativeitrosative stress after lipopolysaccharide (LPS) (endotoxin) administration in an HIV-1 transgenic mouse model. Lung oxidativeitrosative stress biomarkers studied 3 and 6 h after LPS administration were as follows: lung edema, tissue superoxide, NO metabolites, nitrotyrosine, hydrogen peroxide, and bronchoalveolar lavage fluid (BALF) glutathione (GSH). Blood serum cytokine levels were quantified to verify immune function of our nonimmunocompromised animal model. Results indicate that 3 h after LPS administration, HIV-1 transgenic mouse lung tissue has significantly greater edema and superoxide. Furthermore, NO metabolites are significantly elevated in HIV-1 transgenic mouse BALF, lung tissue, and blood plasma compared with those of wild-type mice. HIV-1 transgenic mice also produce significantly greater lung nitrotyrosine and hydrogen peroxide than wild-type mice. In addition, HIV-1 transgenic mice produce significantly less BALF GSH than wild-type mice 3 h after LPS treatment. Without treatment, serum cytokine levels are similar for HIV-1 transgenic and wild-type mice. After treatment, serum cytokine levels are significantly elevated in both HIV-1 transgenic and wild-type mice. Therefore, HIV-1 transgenic mice have significantly greater lung oxidativeitrosative stress after endotoxin administration than wild-type mice, independent of immune function. These results indicate that HIV-1 proteins may increase pulmonary complications subsequent to a secondary infection by altering the lung redox potential.
机译：人类免疫缺陷病毒（HIV）-1通过增加宿主对病原体的敏感性而导致肺部疾病。 HIV-1还导致全身性氧化/亚硝化应激反应增加，可能增强了继发感染的有害影响。在这里，我们检查了在HIV-1转基因小鼠模型中给予脂多糖（LPS）（内毒素）后，HIV-1蛋白增加肺部氧化/亚硝基应激的能力。 LPS给药后3和6小时研究的肺氧化/亚硝化应激生物标记物如下：肺水肿，组织超氧化物，NO代谢产物，硝化酪氨酸，过氧化氢和支气管肺泡灌洗液（BALF）谷胱甘肽（GSH）。量化血清细胞因子水平以验证我们的非免疫受损动物模型的免疫功能。结果表明，LPS给药3小时后，HIV-1转基因小鼠肺组织具有明显更大的水肿和超氧化物。此外，与野生型小鼠相比，HIV-1转基因小鼠BALF，肺组织和血浆中的NO代谢产物明显升高。与野生型小鼠相比，HIV-1转基因小鼠还产生明显更多的肺硝基酪氨酸和过氧化氢。此外，经过LPS处理后3小时，HIV-1转基因小鼠产生的BALF GSH明显少于野生型小鼠。未经治疗，HIV-1转基因和野生型小鼠的血清细胞因子水平相似。治疗后，HIV-1转基因和野生型小鼠的血清细胞因子水平均显着升高。因此，与野生型小鼠相比，HIV-1转基因小鼠在内毒素给药后具有明显更大的肺氧化/亚硝基应激，而与免疫功能无关。这些结果表明，HIV-1蛋白可能通过改变肺氧化还原潜能而增加继发感染后的肺部并发症。

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