SUPPRESSION OF HUMAN PERIPHERAL-BLOOD MONONUCLEAR CELL-FUNCTION BY METHADONE AND MORPHINE
SUPPRESSION OF HUMAN PERIPHERAL-BLOOD MONONUCLEAR CELL-FUNCTION BY METHADONE AND MORPHINE
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DOI：
10.1093/infdis/159.3.480
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发表时间：
1989-03-01
影响因子：
6.4
通讯作者：
SHARP, B
中科院分区：
文献类型：
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作者：
PETERSON, PK;GEKKER, G;SHARP, B
最近的研究表明，外周血单核细胞（PBMC）在体外暴露于吗啡导致单核细胞的增殖爆发活性受到抑制和干扰素-γ受损。（IFN-γ）由淋巴细胞产生。为了研究阿片剂对这些细胞功能的潜在体内作用，从维持美沙酮的患者获得PBMC。这些新鲜分离的单核细胞响应佛波醇肉豆蔻酸酯乙酸酯（PMA）而产生超氧阴离子（O2-）的能力显著受损，而IFN-γ的产生能力显著降低。被伴刀豆球蛋白A刺激的细胞是完整的。细胞培养48 h后，缺陷的O2产生能力得以维持。此外，在浓度低至10-12 M的美沙酮或吗啡存在下，培养来自健康对照的PBMC引起PMA刺激的O2释放的显著抑制。由于PBMC产生的活性氧中间体可能参与艾滋病中宿主对机会致病菌的防御，这些结果强调了研究阿片介导的免疫抑制的生物学后果的必要性。
Recent studies have shown that in vitro exposure of peripheral blood mononuclear cells (PBMC) to morphine results in suppressed respiratory-burst activity of monocytes and impaired interferon-.gamma. (IFN-.gamma.) production by lymphocytes. To investigate the potential in vivo effect of an opiate on these cell functions, PBMC were obtained from patients maintained on methadone. These freshly isolated mononuclear cells had a significantly impaired capacity to generate superoxide anion (O2-) in response to phorbol myristate acetate (PMA), while production of IFN-.gamma. by concanavalin A-stimulated cells was intact. After cell culture for 48 h, the defective O2- generating capacity was sustained. Also, culturing PBMC from healthy controls in the presence of methadone or morphine at concentrations as low as 10-12 M caused significant suppression of PMA-stimulated O2- release. Because reactive oxygen intermediates produced by PBMC may participate in host defense against opportunistic pathogens in AIDS, these results underscore the need for investigations of the biological consequences of opiate-mediated immunosuppression.