The Immune System in COPD
The Immune System in COPD
COPD is the fourth leading cause of death in the U.S. It is a complex respiratory disease with a progressive airflow limitation that is associated with an abnormal inflammatory response. Disease progression is understood in broad terms: airborne respiratory irritants enter the lung and initiate tissue damage. Tissue damage results from a combination of inflammation, oxidative stress, and protease activity. However, for reasons that are unknown, only ~20% of smokers develop significant disease. What are the differences in the inflammatory responses of those that do and do not develop COPD?
Most prior studies of molecular mechanisms in COPD can be classified into two groups: those that study one cell type in great detail (e.g. macrophages) but do not provide information on other cell types, or those that explore immune response in multiple cell types simultaneously but focus on a limited number of proteins, typically a few surface markers. The very term "immune system" suggests that, ideally, one should study multiple immune cell types, with particular attention to the signaling mechanisms used to coordinate their activity. Current mass spectrometry technology allows the identification of hundreds of proteins from a single sample, producing a proteomic profile of the cell. We are investigating proteomic profiles from multiple immune cell types - neutrophils, B-lymphocytes, monocytes, CD4+ and CD8+ T-lymphocytes - from single individuals. The data are both comprehensive across the immune system and rich in molecular detail, and together, provides new insight into inflammation in COPD
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