Abstract
Airway mucus hypersecretion is a feature of many patients with asthma.
It is indicative of poor asthma control and contributes to morbidity and
mortality. Excess mucus not only obstructs airways but also contributes
to airway hyperresponsiveness. Furthermore, asthma might have a specific
mucus hypersecretory phenotype. Goblet cell hyperplasia and submucosal
gland hypertrophy are shared with other hypersecretory diseases, such as
chronic obstructive pulmonary disease; however, some features are
different, including mucus plugging, mucus `tethering' to goblet cells,
plasma exudation, and increased amounts of a low charge glycoform of
mucin (MUC)5B and the presence of MUC2 in secretions. Experimentally,
most of the inflammatory mediators and neural mechanisms implicated in
the pathophysiology of asthma impact upon the mucus hypersecretory
phenotype. There is currently huge research interest in identifying
targets involved in inducing mucus abnormalities, which should lead to
the rational design of anti-hypersecretory drugs for treatment of airway
mucus hypersecretion in asthma.
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