Glutathione depletion in rats impairs T-cell and macrophage immune function.
Glutathione depletion in rats impairs T-cell and macrophage immune function.
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DOI：
10.1001/archsurg.1993.01420130033006
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发表时间：
1993
影响因子：
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通讯作者：
Malcolm K. Robinson;Rodrick Ml;Danny O. Jacobs;Jan D. Rounds;K. Collins;Inna Saporoschetz;J. A. Mannick;Douglas W. Wilmore
中科院分区：
文献类型：
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作者：
Malcolm K. Robinson;Rodrick Ml;Danny O. Jacobs;Jan D. Rounds;K. Collins;Inna Saporoschetz;J. A. Mannick;Douglas W. Wilmore
危重病与免疫抑制和谷胱甘肽缺乏有关。我们确定体内谷胱甘肽的消耗是否会对免疫状态产生不利影响。谷胱甘肽水平正常的大鼠和那些谷胱甘肽商店耗尽马来酸二乙酯进行了脾细胞功能和肠系膜淋巴结淋巴细胞功能的分析。检测脾和肠系膜淋巴结淋巴细胞伴刀豆球蛋白A增殖反应和白细胞介素2产生。还测量了脾粘附细胞的肿瘤坏死因子和白细胞介素6分泌。谷胱甘肽耗竭的动物淋巴细胞增殖显着降低，肿瘤坏死因子和白细胞介素6的产生减少，但白细胞介素2的产生没有改变。这些发现表明，在体内谷胱甘肽缺乏损害巨噬细胞和T细胞的功能。由于谷胱甘肽耗竭可能发生在败血症、创伤和休克中，因此有助于维持谷胱甘肽水平的治疗可能会增强免疫能力，从而提高患者从危重病中恢复的能力。
Critical illness is associated with both immunosuppression and glutathione deficiency. We determined if in vivo depletion of glutathione would adversely affect immune status. Rats with normal glutathione levels and those with glutathione stores depleted by diethyl maleate underwent analysis of splenocyte function and mesenteric lymph node lymphocyte function. Lymphocytes of the spleen and mesenteric lymph nodes were tested for concanavalin A proliferative response and interleukin 2 production. Tumor necrosis factor and interleukin 6 secretion by splenic adherent cells was also measured. Glutathione-depleted animals had significantly decreased lymphocyte proliferation and decreased production of tumor necrosis factor and interleukin 6 but unaltered interleukin 2 production. These findings indicate that in vivo glutathione deficiency impairs macrophage and T-cell function. Because glutathione depletion may occur in sepsis, trauma, and shock, treatments that help maintain glutathione levels may enhance immunocompetence and thus improve the ability of patients to recover from critical illness.