MECHANISMS OF M AVIUM INFECTION IN AIDS

艾滋病中 M AVIUM 感染的机制

• 批准号: 3132420
• 负责人: ALFRED J CROWLE
• 金额: $ 9.2万
• 依托单位: UNIVERSITY OF COLORADO DENVER
• 依托单位国家: 美国
• 财政年份: 1984
• 资助国家: 美国
• 起止时间: 1984-09-30 至 1987-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3132420
• 关键词: AIDS; Actinomycetales infection; Mycobacterium; T lymphocyte; alveolar macrophages; bacterial antigens; bactericidal immunity; cellular immunity; cellular pathology; cytokine; disease /disorder model; growth factor; growth inhibitors; human subject; immune tolerance /unresponsiveness; immunological substance; lymphokines; macrophage; macrophage activating factor; molecular pathology; secondary infection; tissue /cell culture

This project will study cellular and molecular mechanisms of immunodeficiency in acquired immunodeficiency syndrome (AIDS) which account for AIDS susceptibility to opportunistic infection with M. avium. It will use in vitro and in vivo models of antimycobacterial immunity in mice, and in vitro models using human peripheral blood and alveolar cells. Human cells will be obtained from healthy subjects who are PPD-negative or positive to PPD or PPD-Battey, from patients with M. avium infection with or without AIDS, and from AIDS patients without M. avium infection. The project will develop and characterize mouse in vitro and in vivo, and human in vitro cell models of M. avium infection and immunity, study the relative susceptibilities of mouse and human macrophages from different anatomical sites to infection with M. avium, analyse immune lymphokine production and its anti-avium effects in macrophages, and look for factors that may actively impair anti-avium immunity such as the recently discovered mycobacterial growth-enhancing cytokine.

该项目将研究细胞和分子机制 可获得的免疫缺陷综合征（AIDS）的免疫缺陷 用于艾滋病对机会感染的敏感性。 会 在小鼠中使用体外和体内抗菌素免疫模型， 使用人外周血和肺泡细胞的体外模型。 人类 细胞将从PPD阴性或 来自患有大雄性大麻杆菌感染的患者的PPD或PPD - 粉状阳性 或没有艾滋病，也没有艾滋病患者，没有鸟杆菌感染。 这 项目将在体外和体内发展和表征鼠标，人类 体外细胞模型的鸟杆菌感染和免疫力，研究相对 来自不同解剖学的小鼠和人类巨噬细胞的敏感性 用大鸟类感染的部位，分析免疫淋巴因子的产生和 它在巨噬细胞中的抗菌作用，并寻找可能的因素 积极损害抗vavium免疫，例如最近发现的 分枝杆菌增强细胞因子。