Suppr超能文献

吗啡可促进人类外周血单核细胞共培养体系中HIV-1的生长。

Morphine promotes the growth of HIV-1 in human peripheral blood mononuclear cell cocultures.

作者信息

Peterson P K, Sharp B M, Gekker G, Portoghese P S, Sannerud K, Balfour H H

机构信息

Department of Medicine, Hennepin County Medical Center, Minneapolis, MN 55415.

出版信息

AIDS. 1990 Sep;4(9):869-73. doi: 10.1097/00002030-199009000-00006.

Abstract

Because morphine has been shown to alter the function of human T lymphocytes and monocytes, we postulated that morphine would promote the growth of HIV-1 in these cells. To test this hypothesis, a coculture assay was used consisting of phytohemagglutinin (PHA)-activated peripheral blood mononuclear cells (PBMC) from normal donors and PBMC which had been infected with a viral isolate from an asymptomatic patient, HIV-1AT. The growth of HIV-1AT, as reflected by the concentration of p24 antigen in coculture supernatants, was markedly increased in cocultures that contained morphine. A bell-shaped dose-response curve was observed with three- to fourfold increased growth at a morphine concentration of 10(-12) M. Augmentation of HIV-1AT growth by morphine required an interaction with the PHA-activated donor PBMC. Furthermore, potentiation of HIV-1AT growth by morphine was stereospecific and was antagonized by naloxone and beta-funaltrexamine indicating involvement of an opiate receptor mechanism. These findings provide an additional explanation of how opiates could act as a cofactor in the pathogenesis of HIV-1 in intravenous drug users.

摘要

由于吗啡已被证明会改变人类T淋巴细胞和单核细胞的功能,我们推测吗啡会促进HIV-1在这些细胞中的生长。为了验证这一假设,我们采用了一种共培养试验,该试验由来自正常供体的经植物血凝素(PHA)激活的外周血单核细胞(PBMC)和感染了一名无症状患者的病毒分离株HIV-1AT的PBMC组成。如共培养上清液中p24抗原浓度所反映的,HIV-1AT的生长在含有吗啡的共培养物中显著增加。在吗啡浓度为10(-12)M时观察到呈钟形的剂量反应曲线,生长增加了三到四倍。吗啡增强HIV-1AT生长需要与PHA激活的供体PBMC相互作用。此外,吗啡对HIV-1AT生长的增强具有立体特异性,且被纳洛酮和β-氟纳曲胺拮抗,表明涉及阿片受体机制。这些发现为阿片类药物如何在静脉吸毒者中作为HIV-1发病机制的辅助因素提供了另一种解释。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验