Human mononuclear phagocytes from different anatomical sites differ in their capacity to metabolize arachidonic acid.

Human mononuclear phagocytes have the capacity to metabolize arachidonic acid (AA) into prostaglandins (PG) endowed with potent activities in immune responses and inflammatory processes. We have evaluated AA metabolism in human mononuclear phagocytes harvested from different anatomical sites (blood monocytes, macrophages from milk, peritoneal cavity and alveolar spaces). At thin layer radiochromatography, the AA metabolites mainly present were PGE2, TxB2 and, only in bronchoalveolar macrophages, a peak comigrating with PGD2. No appreciable levels of 6-keto-PGF1 alpha were observed. These data were confirmed using specific radioimmunoassays for TxB2, PGE2 and 6-keto-PGF1 alpha. Blood monocytes and bronchoalveolar macrophages were the poorest producers of PG, with the possible exception of PGD2 in bronchoalveolar macrophages. The high amounts of TxB2 and PGE2 produced by milk macrophages could contribute to the levels of PG in human milk. Thus, human mononuclear phagocytes obtained from diverse anatomical sites are considerably heterogeneous in terms of AA metabolism.