The possibility that impaired production of bronchoprotective factors
contributes to the pathogenesis of asthma cannot be excluded. Prostagl
andin E(2) (PGE(2)) could be such a factor. It is a dominant cyclo-oxy
genase product of airway epithelium and smooth muscle; it has inhibito
ry effects on inflammatory cells and pathways involved in bronchoconst
riction at concentrations known to occur in the airway; inhalation of
PGE(2) has considerable bronchoprotective effects in patients with ast
hma; and manoeuvres that increase or decrease endogenous production of
PGE(2) have beneficial and deleterious effects on airway function.