CLINICAL TRIAL: TOBACCO SMOKE INDUCED CELL INJURY IN LUNG COMPARTMENTS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 确定烟草烟雾-TS诱导的肺泡巨噬细胞-AM介导的肺损伤以及α1-抗胰蛋白酶-AAT在调节TS所致肺损伤程度中的保护作用，可能有助于开发更特异的治疗方法来预防或减轻肺损伤。AM是通过上调iNOS产生一氧化氮-NO的来源。在最初的侮辱TS被消除后，不能继续生产很长时间。AAT可能具有抑制肺组织氧化损伤(如iNOS)的功能，这一概念是新的，也是本项目的主题。这是一个试点项目，有20名受试者接受支气管镜检查。将在四个受试组中比较支气管灌洗液、活检/刷检、肺功能测试和研究血液测试：吸烟的健康志愿者、不吸烟的健康志愿者、有记录的慢性阻塞性肺疾病(COPD)患者和阿尔法1抗胰蛋白酶缺陷(AATD)患者。

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. Determining the role of tobacco smoke-TS induced alveolar macrophage-AM mediated lung injury and the protective role of alpha 1-antitrypsin-AAT in modulating the extent of lung injury caused by TS may allow for the development of more specific therapies to prevent or reduce the lung damage. AM are a source of nitric oxide- NO through up-regulation of iNOS. NO production may continue long after the initial insult TS has been eliminated. The concept that AAT may function to inhibit oxidant damage, such as iNOS, to the lung tissue is novel and the subject of this project. This is a pilot project with 20 subjects undergoing bronchoscopy. Bronchial lavage fluid, biopsy/brushings, pulmonary function testing and research blood tests will be compared in four subject groups: healthy volunteers who smoke, healthy volunteers who do not smoke, subjects with documented chronic obstructive pulmonary disease-COPD and subjects with alpha 1-antitrypsin deficiency- AATD.