Protracted increases in core body temperature and interleukin-1 following acute administration of lipopolysaccharide: implications for the stress response.

Administration of lipopolysaccharide (LPS) produces a fever response often precipitated by the production of pro-inflammatory cytokines in the CNS. This pro-inflammatory cascade has traditionally been regarded as a transitory event that, with a non-replicating antigen such as LPS, would subside within a few hours. We present data showing that central and peripheral levels of IL-1 were substantially elevated as much as 48 h after LPS in some structures.

Behavioral responses during the forced swim test are not affected by anti-inflammatory agents or acute illness induced by lipopolysaccharide.

Pro-inflammatory cytokines and other molecules traditionally associated with immune function have been implicated in mediating behavioral and physiological consequences of stressor exposure. There is also evidence that cytokines are aberrantly expressed in depressive populations, suggesting they may play an etiological role in the development of depression/despair-related processes. Thus, we conducted a series of experiments to determine whether agents known to suppress cytokine activity or inflammatory responses in the CNS would alter the normal progression of behavioral responses during the forced swim test (FST, an animal model of depression/behavioral despair).

Exposure to forced swim stress does not alter central production of IL-1.

In recent years, there has been increasing recognition that pro-inflammatory cytokines play a role in behavioral and physiological alterations produced by exposure to psychological stressors. Indeed, increases in central IL-1 production have been observed following stressors such as inescapable tailshock and social isolation, while no changes in IL-1 have been observed following other stressors (e.g.