CONTRIBUTION OF OIS TO INTESTINAL DYSFUNCTION AND WASTING

OIS 导致肠功能障碍和消瘦

• 批准号: 7349495
• 负责人: SAUL r TZIPORI
• 金额: $ 13.48万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7349495
• 关键词: CONTRIBUTION; OIS; INTESTINAL; DYSFUNCTION; WASTING

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A significant loss of CD4+ T cells may be responsible for the development of microsporidiosis and cryptosporidiosis in AIDS patients. SIV infected macaques were used to investigate this relationship. Study on cohort group of macaques showed that spontaneous acquisition of E. bieneusi infection in SIV-infected macaques occurred when their CD4+ counts drops less than 500 cell/ul of blood and increase in viral load, establishing a relationship between E. bieneusi infection and the immune status of SIV-infected macaques. Using C.parvum/SIV co-infection models, SIV-infected macaques develop chronic cryptosporidiosis both during chronic SIV-infection or acute SIV-infection. These studies also indicate that the CD4+ status in the gut mucosa is as, if not more, critical than the peripheral CD4+ level to susceptibility to intestinal pathogens. In contrast, only acute cryptosporidiosis can be induced in SIV-naive macaques. Using E. bieneusi/SIV co-infection model, SIV-infected macaques develop chronic microsporidiosis during chronic SIV-stage.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。CD 4 + T细胞的显著丢失可能是导致艾滋病患者微孢子虫病和隐孢子虫病的原因。SIV感染的猕猴被用来调查这种关系。猕猴队列研究表明，自发获得E。当SIV感染的猕猴的CD 4+计数下降到低于500个细胞/μ l血液和病毒载量增加时，就会发生比纽氏杆菌感染，建立了E. bieneusi感染和SIV感染猕猴的免疫状态。使用微小隐孢子虫/SIV共感染模型，SIV感染的猕猴在慢性SIV感染或急性SIV感染期间均发展慢性隐孢子虫病。这些研究还表明，肠粘膜中的CD 4+状态与外周CD 4+水平对肠道病原体的易感性一样重要（如果不是更重要的话）。相反，只有急性隐孢子虫病可以诱导SIV-幼稚猕猴。使用大肠在bieneusi/SIV共感染模型中，SIV感染的猕猴在慢性SIV阶段发展慢性微孢子虫病。