ABSTRACT
Administration of lipopolysaccharide (LPS), an endotoxin produced by gram-negative bacteria, has been used for several decades in the study of inflammation. This is an easy and simple strategy that induces dose-dependent inflammatory reaction and if given in high doses it may cause systemic inflammatory response syndrome (SIRS) and also death. We have been intrigued by the effects of systemic inflammation for many years, and have been applying this model to the study of central nervous system (CNS) response to systemic inflammation, but we have also been interested in understanding the communications between brain and periphery during systemic inflammation, as intense signs and symptoms mediated by the CNS are initiated by inflammation that originated in the periphery. Those manifestations include suppression of exploration, food intake, and sexual behavior; motor retardation; and alterations in temperature regulation and cognition (1-4); they may result from SIRS and sepsis and have been proposed to be mediated by cytokines, especially interleukin-1 beta (IL-1ß), synthesized during systemic inflammation.
