Prostaglandin E production by human blood monocytes and mouse peritoneal macrophages.

Abstract

Purified populations of both human peripheral blood monocytes and murine peritoneal macrophages synthesize and release Prostaglandin E in vitro. In contrast, prostaglandin E was detected in neither the supernate fluids from cultures of highly enriched human lymphocytes and granulocytes, nor in nonadherent murine peritoneal cells. Macrophage prostaglandin E production was markedly enhanced by endotoxin, and completely suppressed by indomethacin. All neoplastic monocyte-macrophage cell lines examined elaborated prostaglandin E in vitro, either constitutively or after induction with endotoxin. In contrast, prostaglandin E production could not be detected from either a T- or B-cell lymphoma, whether or not they were treated with endotoxin. These findings thus indicate that the blood monocyte and tissue macrophage represent an important source of prostaglandin E, a function shared by both normal and neoplastic mononuclear phagocytes.

Monocytes regulate osteoclast-activating factor production by releasing prostaglandins.

“…Other work from our laboratory has demonstrated that monocytes directly resorb both devitalized bones by a mechanism which is not mediated by the action of osteoclasts (25) and live bones through an osteoclast-mediated mechanism which is prostaglandin-dependent (26). There is also other evidence which suggests that monocytes and macrophages synthesize and release PGs (27)(28)(29), collagenase (30), and hydrolytic enzymes (31), which are all capable of resorbing bone or degrading bone matrix. It is also possible that circulating mononuclear cells may transform or differentiate into osteoclasts (32).…”

IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons gamma and alpha and prostaglandin E2.

“…IFN-a tested alone was ineffective. IFN-q and PGE2 are known to be produced by monocytes (21,22), which therefore may account for the suppression of IgE production observed in the presence of relatively high monocyte concentrations (data not shown). These data indicate that factors that inhibit CD23 induction by IL-4 on B cells also blocked IL-4-induced IgE production, which suggests an assoqiation between CD23 expressed on B cells and IgE production.…”

Immunological tolerance induced by liver grafting in the rat: splenic macrophages and T cells mediate distinct phases of immunosuppressive activity

“…Of particular importance is the ability of macrophages to act as a source of prostaglandins, which are potent inhibitors of several lymphocyte functions, such as mitogenesis (Goodwin, Bankhurst & Messner, 1977), cytolysis (Lichtensteine; a/., 1972; Koga et al, 1982), lymphokine production (Gordon, Bray & Morlcy, 1976), and proliferation (Stout & Fisher, 1982). The principal inhibitory prostaglandins released by suppressor macrophages appears to be those ofthe E series (PGEi, PGE2) (Humes et al, 1977;Kurland & Bockman, 1978;Stenson & Parker, 1980), the production of which is blocked by indomethacin. Our results thus provide a further example of the correlation between a suppressive effect of macrophages and their ability to release prostaglandins; they suggest a role for both in modulating liver graft rejection in the critical period after grafting when tolerance is becoming established.…”