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Airways Inflammation and COPD*: Epithelial-Neutrophil Interactions

Carol A. Pettersen, MS; Kenneth B. Adler, PhD
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*From the Department of Anatomy, Physiological Sciences & Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.

Correspondence to: Kenneth B. Adler, PhD, Professor of Cell Biology, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough St, Raleigh, NC 27606; e-mail: Kenneth_Adler@ncsu.edu



Chest. 2002;121(5_suppl):142S-150S. doi:10.1378/chest.121.5_suppl.142S
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Neutrophils are recognized as major cellular mediators of inflammation. They contain specific and highly regulated mechanisms for controlling the expression of adhesion molecules that allow for their tethering and migration into inflammatory sites. These adhesion molecules not only are activated by exogenous pollutants but are regulated by endothelial and epithelial cell signals. Lipid mediators, such as platelet-activating factor, reactive oxygen and nitrogen species, and cytokines from airway epithelial cells, further control neutrophil functions such as infiltration and activation resulting in an increase in respiratory burst activity and release of granule enzymes, such as elastase. Furthermore, virus and bacteria products affect inflammation by increasing secondary epithelial mediators. However, once the endogenous or exogenous agents are expelled, neutrophil populations are programmed to die and are cleared by macrophage phagocytosis.


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