ABSTRACT
This chapter attempts to establish causal roles for interleukins in the development of septic shock in vivo and to assess qualitatively and quantitatively the relevance of each of these mediators to therapeutic approaches. Cytokines are regulatory proteins released from a wide variety of cells, although in sepsis macrophages are the most important source. Studies performed in the early 1980s provided evidence that the host’s reticuloendothelial system generated the signals that induced the adverse responses following Gram-negative infection. The intravenous administration of cytokines may not necessarily be illustrative of pathophysiologic events, but could be merely pharmacological effects following drug administration. Lipopolysaccharides trigger many of the pathophysiologic events associated with Gram-negative bacterial sepsis. The clinical signs and symptoms after Interleukin-2 administration could be characterized as “flu-like” and were qualitatively and quantitatively indistinguishable from those that occurred after endotoxin administration in healthy subjects, albeit with a different time course.
