Prostaglandin E2, prostaglandin E1 and thromboxane B2 release from human monocytes treated with C3b or bacterial lipopolysaccharide

Abstract

C3b or lipopolysaccharide treatment of human peripheral blood monocytes in culture stimulates an early release of thromboxane B2 and a delayed release of prostaglandin E into culture supernatants. Immunoreactive thromboxane B2 release is maximal from 2-8 h, whereas prostaglandin E release is maximal from 16-24 h after stimulation of monocytes in culture. We further examined this process by comparing the time course of labelled prostaglandin E2, prostaglandin E1 and thromboxane B2 release from human monocytes which were pulse or continuously labelled with [3H]arachidonic acid and [14C]eicosatrienoic acid. The release of labelled eicosanoids was compared with the release of immunoreactive prostaglandin E and thromboxane B2. The time course of prostaglandin E2 release was virtually identical to the release of prostaglandin E1 in all culture supernatants regardless of labelling conditions. However, release of immunoreactive prostaglandin E paralleled the release of labelled prostaglandin E1 and E2 only for continuously labelled cultures. The release of labelled prostaglandin E1 and E2 from pulse labelled cultures paralleled the release of thromboxane B2 and not immunoreactive prostaglandin. In contrast, labelled and immunoreactive thromboxane B2, quantitated in the same culture supernatants, demonstrated similar release patterns regardless of labelling conditions. These findings indicate that the differential pattern of prostaglandin E and thromboxane B2 release from human monocytes is not related to a time-dependent shift in the release of prostaglandin E1 relative to prostaglandin E2. Because thromboxane B2 and prostaglandin E2 are produced through cyclooxygenase mediated conversion of arachidonic acid, these results further suggest that prostaglandin E2 and thromboxane B2 are independently metabolized in human monocyte populations.