TROPICAL DISEASE RESEARCH UNITS

热带病研究单位

• 批准号: 3091454
• 负责人: ADEL A. MAHMOUD
• 金额: $ 62.91万
• 依托单位: CASE WESTERN RESERVE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-07-01 至 1990-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3091454
• 关键词: filariasis; immunity; onchocerciasis; schistosomiasis; tropical medicine

During the past year, this multidisciplinary program project on parasitic infections continued studies aiming at elucidating the pathogenic and modulating mechanisms in the following areas: 1. In schistosomiasis, the protective function of the eosinophil within the host granulomatous response surrounding S. mansoni eggs has been defined. In the absence of these cells, eggs accumulate in the host tissues causing considerable morbidity. Studies on S. japonicum infection resulted in understanding the course of pathophysiological modulation and the underlying mechanism of decreased disease in chronically infected mice. Furthermore, the specific glycoprotein S. japonicum egg antigens responsible for sensitization for granuloma formation and elucidation of immediate hypersensitivity have been isolated and characterized. 2. In giardiasis, the dynamics and characteristics of immunity passively transferred from mothers to their offspring have been delineated. These changes were reproduced by injecting sex hormones in female mice. In addition, the localization of the organism and histopathologic changes in the intestines of G. muris infected mice were studied. 3. Immunologic investigations aimed at defining the interaction of macrophages, lymphocytes, serum borne factors and the parasites as they contribute to immune response and its regulation in human and experimental schistosomiasis. Studies were carried out in Egypt and Cleveland to evaluate the suppressor splenic cells, the immune response to worm antigens and monocyte mediated killing of schistosomula in human schistosomiasis. Furthermore, the mechanism of augmented schistosomula killing by activated macrophages have been described.

在过去的一年里，这个关于寄生虫的多学科项目 感染继续研究，旨在阐明其致病机理和调控机制 机制如下：1.在血吸虫病中，保护性 嗜酸性粒细胞在宿主肉芽肿性反应中的作用 曼氏虫卵已被定义。在没有这些细胞的情况下，卵就会积累起来 在宿主组织中造成相当大的发病率。日本血吸虫的研究 感染导致对病理生理调节过程的理解 以及慢性感染小鼠疾病减少的潜在机制。 此外，日本血吸虫虫卵抗原的特异性糖蛋白 用于肉芽肿形成的致敏作用和阐明即刻 超敏反应已被分离和鉴定。2.在贾第鞭毛虫病中， 母体免疫被动转移的动态及特点 它们的后代已经被描绘出来了。这些变化是由 给雌性小鼠注射性激素。此外，本地化 小鼠感染革兰氏原虫后肠道的组织病理学变化 ，并对其进行了研究。3.旨在确定相互作用的免疫学调查 巨噬细胞、淋巴细胞、血清传播因子和寄生虫 在人体和实验中对免疫应答及其调节的贡献 血吸虫病。在埃及和克利夫兰进行了研究，以评估 抑制性脾细胞，对蠕虫抗原和单核细胞的免疫反应 人血吸虫病的介导性杀灭血吸虫幼虫。此外， 激活的巨噬细胞增强杀灭血吸虫的机制已被证实 描述。