FIG. 1.

Schematic representation of the balance between pro- and anti-inflammatory cytokines elicited during bacterial sepsis. The onset of bacterial sepsis immediately leads to the production of numerous proinflammatory mediators, such as TNF-α, IL-1β, IL-6, IL-8, and NO. To prevent an overwhelming inflammatory response anti-inflammatory mediators such as IL-10 and MCP-1 are produced a few hours later. These cytokines have pleiotropic effects functioning to directly inhibit proinflammatory cytokine synthesis and promote the synthesis of specific cytokine inhibitors, such as IL-1 receptor antagonist and soluble TNF receptors. In addition, they downregulate chemokine and chemokine receptor production and inhibit Th1 cytokines, such as IL-2 and IFN-γ.