TOBACCO SMOKE INDUCED CELL INJURY IN LUNG COMPARTMENTS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 确定烟草烟雾（TS）诱导的肺泡巨噬细胞（AM）介导的肺损伤的作用和α 1-抗胰蛋白酶（AAT）在调节由TS引起的肺损伤程度中的保护作用，可能允许开发更特异性的治疗以预防或减轻肺损伤。 AM是通过上调iNOS产生一氧化氮（NO）的来源。 NO的产生在初始污染物（TS）被消除后很长一段时间内可能会继续。AAT可能具有抑制氧化剂损伤（如iNOS）对肺组织的作用，这一概念是新颖的，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4个受试者组-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）受试者和α 1-抗胰蛋白酶缺乏症（AATD）受试者中比较支气管灌洗液、活检/刷检、肺功能检测和研究血液检测。

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).