Arachidonic acid metabolism is altered in sarcoid alveolar macrophages.

Macrophages produce various arachidonic acid (AA) metabolites which may either enhance or suppress inflammatory processes. We investigated AA metabolite production by alveolar macrophages (AMs) from 11 patients with pulmonary sarcoidosis and 9 normal volunteers. We assessed the production of both cyclooxygenase products (prostaglandin (PG) E2, thromboxane B2 (TXB2), PGF2 alpha, and 6-keto-PGF1 alpha) and lipoxygenase products (leukotrienes (LT) and hydroxyeicosatetraenoic acids (HETEs] in AM cultures. We found that sarcoid AMs produced less PGE2, TXB2, 6-keto-PGF1 alpha, and HETEs in both the unstimulated and the calcium ionophore-stimulated states compared with normal AMs. Sarcoid AMs also produced less PGF2 alpha and LTs in the unstimulated state after 1 hr of incubation, but following calcium ionophore stimulation, these differences did not achieve statistical significance. We conclude that sarcoid AMs have a reduced capacity to produce AA metabolites compared with that of normal AMs.