The inflammatory process is a vital response to injury, infection, trauma, and many other insults. For a successful outcome after injury (including surgically induced trauma), the inflammatory response must be triggered to bring about recruitment of blood leukocytes, activation of tissue macrophages, and production of a series of mediators. The results of this may include ultimate resolution of the inflammatory process, triggering events that lead to cell regeneration and wound healing, or progression of the inflammatory response, which often leads to progressive organ dysfunction. Understanding how the inflammatory process is activated and how it is contained are key to developing strategies designed to block or reduce inflammatory responses, similar to immunosuppressive interventions when immune responses are unwanted (eg, allograft rejection) or exaggerated (eg, autoimmune responses). A good example of an undesirable inflammatory response occurs in the "systemic inflammatory response syndrome" during sepsis. In this situation, cytokines (eg, interleukin 1 [IL-1], IL-6, tumor necrosis factor α [TNF-α]) are detectable in the plasma, suggesting unregulated generation of these highly inflammatory peptides.1 Under such conditions multiorgan failure often occurs. What remains to be determined is why, during sepsis, there is uncontrolled production of cytokines and how these cytokines may be involved in multiorgan failure.