Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA 91766, USA.
J Interferon Cytokine Res. 2013 May;33(5):270-9. doi: 10.1089/jir.2012.0103. Epub 2013 Feb 14.
In this study, we determined the effects of glutathione (GSH)-enhancing agents in restoring the levels of GSH in isolated macrophages from individuals with HIV infection thereby resulting in improved control of Mycobacterium tuberculosis. Our results indicate that treatment with N-acetyl cysteine or a liposomal formulation of glutathione (lGSH) resulted in replenishment of reduced also known as free GSH (rGSH), and correlated with a decrease in the intracellular growth of M. tuberculosis. Finally, we observed differences in the amount of the catalytic subunit of glutamine-cysteine ligase (GCLC), glutathione synthase, and glutathione reductase present in macrophages derived from healthy and HIV-infected individuals. These changes correlated with changes in free radicals as well as rGSH levels. Our results indicate that HIV infection leads to increased production of free radicals and decreased production of GCLC resulting in depletion of rGSH and this may lead, in part, to the loss of innate immune function observed in HIV patients. These findings represent a novel mechanism for control of M. tuberculosis infection, and a possible supplement to current HIV treatments.
在这项研究中,我们确定了谷胱甘肽 (GSH) 增强剂在恢复 HIV 感染个体分离的巨噬细胞中 GSH 水平方面的作用,从而导致对结核分枝杆菌的更好控制。我们的结果表明,用 N-乙酰半胱氨酸或谷胱甘肽的脂质体制剂(lGSH)治疗可补充还原型也称为游离 GSH(rGSH),并与结核分枝杆菌的细胞内生长减少相关。最后,我们观察到来自健康个体和 HIV 感染者的巨噬细胞中谷氨酰胺半胱氨酸连接酶 (GCLC)、谷胱甘肽合酶和谷胱甘肽还原酶的催化亚基的量存在差异。这些变化与自由基以及 rGSH 水平的变化相关。我们的结果表明,HIV 感染导致自由基产生增加和 GCLC 产生减少,导致 rGSH 耗尽,这可能部分导致 HIV 患者观察到的先天免疫功能丧失。这些发现代表了控制结核分枝杆菌感染的新机制,可能是目前 HIV 治疗的补充。