Abstract
Antigen challenged alveolar macrophages (ac-AM) showed much higher basal prostagtandin E 2 (PGE 2) release (4.4-fold) and cAMP content (2.4-fold) than naive alveolar macrophages (AM). In naive AM 1 fM platelet activating factor (PAF) enhanced PGE 2 release from 115 to 157 ng/5 × 10 6cells but was inactive at 1 nM or 1 μM. In ac-AC 1 fM PAF enhanced PGE 2 release from 510 to 670 ng/5 × 10 6 cells and inhibited leukotriene B 4 (LTB 4) release (from 6.0 to 4.8 ng/5 × 10 6 cells). At a 10 6-fold higher concentration PAF inhibited PGE 2 release (from 510 to 400 ng/5 × 10 6 cells) and stimulated LTB4 release (from 6.0 to 8.2 ng/5 × 10 6 cells). PAF-induced increase or decrease in PGE 2 release was paralleled by changes in cellular cAMP (+35 and −17%, respectively). The specific PAF-antagonist BN 52021 completely reversed all PAF-induced effects while indomethacin inhibited only PAF-induced increase in PGE 2 release and cAMP leaving LTB 4 release unaffected. Similarly, the lipoxygenase inhibitor AA-861 inhibited PAF-induced rise in LTB 4 release leaving the enhancement in PGE 2 release and cAMP content unaffected. Present data show that PAF dose-dependently affects eicosanoid production and cAMP level in alveolar macrophages.
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