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to certain groups of patients, particularly those that are prone to respiratory
tract infection. Nevertheless, it is important to develop drugs that inhibit
mucus hypersecretion in these susceptible patients. However, before addres-
sing these issues in a rational manner, considerably more information is
required on basic mucus physiology and, in particular, mucus pathophysiol-
ogy. For example, more detail is required concerning the biochemical and
biophysical nature of airway mucins in normal healthy subjects. Answers
to the questions of whether or not there is an intrinsic abnormality of mucus
in COPD, and whether any abnormality is specific for COPD are urgently
required. In addition, the factors that regulate MUC gene expression in
health and disease, and the relationship between this regulation and devel-
opment of a hypersecretory phenotype that appears to be specific to the
bronchitic component of COPD, need to be determined. The above infor-
mation could then be used in delineation of therapeutic targets which, in
turn, should lead to rational design of anti-hypersecretory drugs for specific
treatment of airway mucus hypersecretion in COPD.
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