Abstract
Intra-tracheal administration of PAF-acether (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) to guinea-pigs induces a bronchoconstriction, which appears to depend on the cell population located in the bronchi, mainly alveolar macrophages [1]. In addition, the exposure of alveolar macrophages in vitro to PAF-acether results in an increased liberation of arachidonic acid (AA) from phosphatidylcholine and phosphatidyl-inositol, suggesting the activation o fPLA 2 or PLC in concert with diglyceride lipase activities [2]. Activation of macrophages is known to be suppressed by PGE 2 and /r agonists because of their ability to elevate intracellular cAMP (cyclic AMP) concentrations [3]. Considering these findings, and in view of the hypothetized role of PAF-acether and alveolar macrophages in asthma, we examined the possible involvement of cAMP levels for controlling the effects of PAF-acether in alveolar macrophages.
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