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.
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