Arachidonic acid metabolism in alveolar macrophages. A comparison of cells from healthy subjects, allergic asthmatics, and chronic bronchitis patients.

Arachidonic acid (AA) metabolism was studied in preparations of purified human alveolar macrophages (AM) from healthy subjects (HS = 5), allergic asthmatics (ABA = 9) and chronic bronchitis patients (CB = 7). AM incubated for 6 to 24 h in the presence of labeled AA and for an additional 5 h without labeled AA, released cyclooxygenase and lipoxygenase products into the medium. The study of the metabolites showed that the most abundant sulfidopeptide-leukotriene, was LTD4 as analyzed by TLC and identified by reversed phase HPLC. The release of LTD4 was time-dependent but it was shown to be significantly higher (p less than 0.01) in AM from ABA or CB than in those from HS. TLC analysis of radioactivity distributed between the different lipid classes at 24 h revealed more labeling in AM phospholipids from ABA and CB than in those from HS, and was reflected in phosphatidylethanolamine and phosphatidylinositol species. After 5 h without labeled AA the distribution was marked, by different in triglycerides, with a greater proportion of radioactivity in the control cells than in the pathological macrophages. Thus, the pathological lung state is an important factor affecting the release of LTD4 and the distribution of AA into cellular phospholipids. The differences observed between HS and ABA or CB phospholipid distribution suggests the existence of 2 different sources of AA release, one for inflammatory macrophages and another for quiescent cells.