FIG. 8.

Model for how PTx, arachidonic acid metabolites, TNF-α, and PAF modulate the synthesis or secretion of IL-1β in macrophages stimulated by TxA from C. difficile. In this model, TxA interacts with a G-protein-linked receptor present in the macrophage membrane and induces the release of inflammatory mediators, such as prostaglandins (PGs), PAF, and TNF-α. These mediators might stimulate the macrophages to secrete IL-1β in an autocrine manner. In addition, proteolytic activity is needed during the formation of IL-1β. This scheme also shows that potential pharmacological blockers, such as cyclo-oxygenase products, PAF, TNF-α, and protease inhibitors, could affect the synthesis and release of this cytokine.