榊原 博樹

Prostaglandin E2 (PGE2) is produced by resident cells in the airway, such as airway epithelial cells, airway smooth muscle cells and alveolar macrophages, and is always present in the airway. Various exogenous and endogenous stimuli cause immediate increases in PGE2 from several-fold to multiples of 10-fold. Prostaglandin E2 controls the function of cells that contribute to immune and inflammatory responses, such as lymphocytes, eosinophils, mast cells, macrophages and polymorphonuclear cells, and exhibits suppressor activity in the initial and advanced stages of allergic airway inflammation (establishment of sensitization, induction of early asthmatic response, chemotaxis of inflammatory cells and continuation of the late asthmatic response). Therefore, if the endogenous protective effects of PGE2 are weakened or absent, inflammation and hypersensitive responses readily occur in the airway. Although the effects of PGE2 remain to be clarified, the possibility of the involvement of decreased PGE2 activity in the pathogenesis of asthma exists. However, in aspirin-induced asthma the role of PGE2 as a protective factor, through an as yet undetermined mechanism, is marked. It is thought that, in this type of asthma, symptoms may be induced by the elimination of the protective action of PGE2 by non- steroidal anti-inflammatory drugs (NSAID). It is possible that PGE2 agonists that produce little airway irritation and drugs that raise the endogenous PGE2 level have potential as new types of anti-inflammatory or anti-asthma drugs.