Alveolar macrophage proteomics in HIV-induced emphysema

HIV 引起的肺气肿中的肺泡巨噬细胞蛋白质组学

• 批准号: 7125473
• 负责人: Philip T Diaz
• 金额: $ 40.15万
• 依托单位: OHIO STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-09-29 至 2010-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7125473
• 关键词: AIDS therapy; HIV infections; alveolar macrophages; antiviral agents; biotechnology; clinical research; combination chemotherapy; computed axial tomography; disease /disorder proneness /risk; emphysema; host organism interaction; human immunodeficiency virus 1; human subject; inflammation; latent virus infection; lung imaging /visualization /scanning; lung injury; lung lavage; medical complication; microorganism immunology; pathologic process; proteomics; respiratory gas transport; smoking; virus infection mechanism

DESCRIPTION (provided by applicant): Evidence exists that HIV-seropositve smokers are at increased risk for developing pulmonary emphysema. Understanding the natural history of this phenomenon has important implications regarding lung disease in the setting of HIV. Furthermore, delineating important molecular mechanisms responsible for this accelerated process may have broad relevance regarding emphysema pathogenesis. In order to gain better insight into HIV- associated emphysema the current proposal seeks to address two specific aims: Specific Aim 1. To delineate the natural history of HIV-associated emphysema in the HAART era. In this aim we will test the hypothesis that parenchymal lung damage is attenuated in the HAART era. We will also examine the progression of physiologic abnormalities among a well characterized group with prominent gas exchange alterations. Specific Aim 2. In this aim we will compare the proteomes of alveolar macrophages obtained from HIV-seropositive smokers with and without emphysema. Successful completion of this project will enable us to further delineate the importance of smoking related lung damage occurring in the HIV-seropositive population. More importantly, the research proposed in this proposal will provide a unique opportunity to examine relevant mechanisms underlying the progression of early emphysema.

描述（由申请人提供）： 有证据表明，艾滋病毒血清阳性吸烟者患肺气肿的风险增加。了解这种现象的自然史对于艾滋病毒背景下的肺部疾病具有重要意义。此外，描述导致这一加速过程的重要分子机制可能与肺气肿发病机制具有广泛的相关性。为了更好地了解 HIV 相关肺气肿，当前提案旨在解决两个具体目标： 具体目标 1. 描述 HAART 时代 HIV 相关肺气肿的自然史。为此，我们将检验 HAART 时代肺实质损伤减轻的假设。我们还将检查一组具有显着气体交换变化的特征明确的生理异常的进展情况。具体目标 2。在此目标中，我们将比较从患有和不患有肺气肿的 HIV 血清阳性吸烟者获得的肺泡巨噬细胞的蛋白质组。该项目的成功完成将使我们能够进一步阐明艾滋病毒血清阳性人群中吸烟相关肺损伤的重要性。更重要的是，该提案中提出的研究将为检查早期肺气肿进展的相关机制提供独特的机会。