In addition to central neuropathological consequences, TBI has humoral neural signs, such as elevated circulating levels of catecholamines, which contribute to the immunosuppression observed in patients with TBI by inducing the release of the immunosuppressive cytokine, IL-10. Therefore, the central insult provoked by TBI has clinically significant sequelae in that it puts the patients at increased risk for depressed immune surveillance, infection and sepsis (Plata-Salaman 1998; Woiciechowsky et al. 1998). In point of fact, inflammation is a critical aspect of the central and peripheral response to TBI. The process by which the central and the peripheral responses interact constitutes an important part of the pathophysiology of TBI, and is regulated in large part by the blood-brain barrier. Numerous immune mediators released within minutes of the primary injury determine and guide the neuroimmune sequence of events that follows, and its protraction in time (Morganti-Kossmann, Rancan, Stahel, and Kossmann 2002). Cytokines, such as interleukin (IL)-ip, tumor necrosis factor (TNF)-a and IL-6, released from antigen-activated immune cells, are the chief messengers of afferent signals that cross the blood--brain barrier and play a key role as regulators of the host-defense response (Besedovsky and Del Rey 2001) as well as sleep disorders (Vgontzas, Bixler, Lin, Prolo, Trakada, and Chrousos 2005).
Like the hormonal response to stress, the cytokine reaction is fundamental for survival. Through a variety of mechanisms, the brain detects activation of the peripheral immune system. The brain responds to infection by altering physiological processes and complex behavior, including sleep. These changes in physiology and behavior collectively function to support the immune system, and under normal circumstances the health of the host is restored (Prolo and Chappelli in press). Several of these cytokines, and their receptors, are present in normal healthy brain. Other cytokines, such as IL-6, regulate sleep under physiological conditions, in the absence of infection or immune challenge.
For example, IL-1 directly alters discharge patterns of neurons in hypothalamic and brainstem circuits implicated in the regulation of sleep-wake behavior (Alam et al. 2004). Other cytokines, such as IL-6, modulate sleep because they interact with neurotransmitter, peptide, and/or hormone systems to initiate a cascade of responses that subsequently alter sleep-wake behavior. Blood levels of IL-6 correlate with sleep and sleepiness, and its circadian pattern mirrors the homeostatic drive to sleep (Vgontzas et al. 2005). Because cytokines regulate/modulate sleep-wake behavior in the absence of immune challenge, and cytokine concentrations and profiles are altered during infection, it is likely that cytokines mediate infection-induced alterations in sleep.
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