Abstract
Sickness behavior refers to a coordinated set of behavioral changes that develop in sick individuals during the course of an infection. These changes are due to the effects in the brain of proinflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFα) and represent the expression of a well-organized central motivational state. Based on the results of pharmacological and biochemical experiments, it is now apparent that sickness behavior is mediated by cytokines that are temporarily synthesized and released in the brain during infection. These cytokines act on brain receptors that are identical to those characterized on immune cells. Primary afferent nerves represent the main communication pathway between peripheral and central cytokines. The existence of a brain cytokine compartment that is inducible by peripheral immune stimuli and is associated with sickness behavior has important pathophysiological implications.
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