Abstract
We identified the probable intermediate step in the suppression of tumor-necrosis factor (TNF) synthesis by prostaglandin E2 or phosphodiesterase (PDE) inhibitors. This step serves as a tool in further studies of the mechanisms of TNF-gene regulation. Furthermore, suppression of TNF synthesis may contribute to the beneficial effects of PDE inhibitors in animal models of septic shock or lung injury and may thus have clinical implications.