Sickness-induced Cognitive Dysfunction: Molecular, Physiological, and Behavioural Correlates

Activated immune cells secrete proinflammatory cytokines that induce a generalized sickness response. The following experiments were designed to determine whether the proinflammatory cytokine IL-1β is the peripheral mediator of sickness-induced cognitive dysfunction, as well as to characterize the cognitive processes that are disrupted during illness. The effects of peripherally-administered IL-1β and LPS, an endotoxin that induces a peripheral immune response, are compared across learning and memory tasks, and on hippocampal LTP. LPS impaired memory consolidation and inhibited EPSP expression, whereas IL-1β had no effects across tasks, nor on LTP expression. However, IL-1β plus IL-6, inhibited hippocampal cell proliferation. Therefore, sickness-induced cognitive dysfunction is characterized by a disruption of memory consolidation and an inhibition in hippocampal LTP. In addition, whereas peripheral IL-1β, alone, is insufficient to disrupt learning and memory or hippocampal physiology, it may work with other proinflammatory cytokines, such as IL-6, to produce effects in the CNS.