Abstract
A common feature of COPD and other chronic lung diseases is hypersecretion of mucus into the airways, causing peripheral airway plugging and further airflow obstruction. The mucus is secreted by goblet cells, which are present in excessive numbers in COPD. This review describes how neutrophils in the airways of COPD patients stimulate the goblet cells to secrete their products. Recent findings on the mechanisms of neutrophil stimulation of goblet cell degranulation are discussed. These implicate the proteolytic enzyme elastase and cell surface adhesion molecules, and provide a basis for the investigation of potential novel therapies.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Biomarkers
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Cell Movement / drug effects
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Chemotactic Factors / therapeutic use*
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Goblet Cells / drug effects
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Goblet Cells / metabolism
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Goblet Cells / pathology
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Humans
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Leucine / analogs & derivatives
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Leucine / therapeutic use
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Leukocyte Elastase / antagonists & inhibitors
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Leukocyte Elastase / metabolism*
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Lung Diseases, Obstructive / drug therapy*
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Lung Diseases, Obstructive / enzymology*
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Lung Diseases, Obstructive / pathology
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Mucus / enzymology
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Neutrophils / drug effects
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Neutrophils / enzymology
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Neutrophils / metabolism*
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Recurrence
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Respiratory System / metabolism*
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Respiratory System / pathology
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Treatment Outcome
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Biomarkers
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Chemotactic Factors
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N-(9H-(2,7-dimethylfluoren-9-ylmethoxy)carbonyl)leucine
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Leukocyte Elastase
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Leucine