To explore potential proteins that may be used to develop novel therapies for COPD. This
will be accomplished by acquiring material from the lower respiratory tract via
Chronic Obstructive Pulmonary Disease(COPD) is currently the fourth leading cause of death
in the United States. COPD is characterized by reduced airflow that is largely irreversible
and progressive. Smoking is recognized as the most important cause of COPD contributing up
to 80% of the cases. The disease does demonstrate a significant variability in airflow
obstruction during the progression of the disease among those who are diagnosed and treated.
This is probably due not only to the role of exposure of cigarette smoke and other noxious
inhaled particles and gases but also to the individual's varied responses to those
COPD is characterized by an inflammatory response that does have a number of components that
may be present in variable amounts. Recent data suggests that the cigarette exposure may
cause several distinct pathophysiological processes that in turn may account for the
variability demonstrated in altered lung structure that leads to functional impairment.
Current therapies can help with alleviation of symptoms in individuals but not the unaltered
course of loss in lung function that frequently leads to respiratory failure and death.
New strategies have been discussed as a means to new therapeutic approaches to altering the
course of the disease. The use of genomic and proteomic methodologies offer promise to
identify the pathways critical and relevant to the progression of COPD. To date approved
medications target only the inflammatory response to the disease.
The study will explore metabolic pathways that could affect the remodeling process
associated with the disease. Because of the heterogeneity of COPD, characteristics of the
individual as well as between individuals must be identified in more detail. Mechanisms that
enable this not only include physiological characterization by the current prescribed
interventions but also imaging data which provides such ability to quantify airway wall
thickness as well as via DNA that will be collected and save in order to gain a better
understanding between the methodologies as they relate to the characterization of COPD.
Currently, there may be a common understanding of how a particular drug affects a detailed
molecular mechanism, however frequently it is not known why. The purpose of this study is to
assist in discovery of the why.
- Age 45-70 yrs of age, incl, women as described above as far as child-bearing
potential and subjects who if they have coexisting disease, the disease is stable and
does not place an untoward risk or result in compromise of data.
- Non smokers will be lifelong and have not worked in a chronic dusty environment.
- Smokers will require a minimum of 10 pkyr history and currently smoking at least a
pack per day. The smokers without symptoms of COPD must demonstrate a pulmonary
function with an FEV1 > 80%. The FEV1/FVC ratio may be less than .7 however they can
not demonstrate symptoms of chronic bronchitis by medical history. Smokers with
symptoms must demonstrate an FEV1 < 80% and FEV1/FVC <.7.
- Any female subject who is pregnant or breast-feeding or a female subject who is of
child-bearing potential who is unwilling to sue two acceptable methods of birth
- Any condition that would place the subject at risk for endobronchial brushings(such
as bleeding diathesis) or subjects who are currently taking anticoagulants.
- Any subject who has had an exacerbation of COPD within the last six months of
screening or who has been hospitalized for any reason within the last three months.
- Illicit substances indicated by positive urine drug screen.