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Airways inflammation and COPD: Epithelial-neutrophil interactions
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Airways inflammation and COPD: Epithelial-neutrophil interactions
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Conference Proceeding
Airways inflammation and COPD: Epithelial-neutrophil interactions
2002
Overview
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.
Publisher
American College of Chest Physicians
Subject
/ Biological and medical sciences
/ Cell Adhesion Molecules - metabolism
/ Chronic obstructive pulmonary disease, asthma
/ Humans
/ Inflammation - physiopathology
/ Inflammation Mediators - metabolism
/ Ligands
/ Neutrophil Activation - immunology
/ Pulmonary Disease, Chronic Obstructive - immunology
/ Respiratory Mucosa - immunology
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