EARLY IMMUNE EVENTS IN CHILDHOOD ASTHMA

儿童哮喘的早期免疫事件

• 批准号: 8357279
• 负责人: LISA M MILLER
• 金额: $ 7.56万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357279
• 关键词: California; Childhood Asthma; Clinical; Development; Event; Funding; Grant; Immune; Lung; Macaca mulatta; Modeling; National Center for Research Resources; Primates; Principal Investigator; Pulmonary Eosinophilia; Research; Research Infrastructure; Resources; Source; Symptoms; United States National Institutes of Health; allergic airway disease; cost; postnatal

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The primary objective of this project is to determine the early pulmonary mechanisms that initiate development of clinical symptoms in childhood asthma, using a rhesus monkey model of allergic airways disease. We have hypothesized that pulmonary eosinophilia is a critical first step in the initiation of allergic airways disease during postnatal development.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 本项目的主要目的是使用过敏性气道疾病的恒河猴模型，确定儿童哮喘临床症状发生的早期肺机制。 我们假设肺嗜酸性粒细胞增多是出生后过敏性气道疾病发生的关键第一步。