Are prostaglandins proinflammatory, antiinflammatory, both or neither?

Research on the role of prostaglandins (PG) in inflammation has been divided along 2 lines of inquiry. One supposes that PG are proinflammatory, explaining why nonsteroidal antiinflammatory drugs (NSAID), which prevent conversion of arachidonic acid to stable PG through cyclooxygenase inhibition, exert their antiinflammatory effects. The other supposes that PG are antiinflammatory, explaining the reductions in inflammation produced by these substances in various experimental models of arthritis. A number of proinflammatory actions of PG have been identified, including vasodilatation and hyperalgesia. However, these activities are relatively modest and do not appear to account for the antiinflammatory effects of NSAID; indeed, mechanisms for these effects that do not depend on cyclooxygenase inhibition have been advanced. A number of potential mechanisms for antiinflammatory effects of PGE have been identified, including inhibition of neutrophil activation, O2 release and leukotriene B4 and cytokine production. It is likely that the availability of orally active PGE analogs will permit study leading to an integrated understanding of PG activity and an answer to the question whether such agents will prove useful in the treatment of chronic inflammatory diseases.