Introduction

It is a truism that sleep remains an important enigma in neurobiology and physiology. It is trite to acknowledge that sleep clearly has an important adaptive value to the organism as a whole, yet defining that function remains elusive (Krueger, Majde, and Obal 2003; Siegel 2003). One prominent thought has been that sleep promotes recovery from infectious challenge. Consistent with this notion are the common observations of lethargy and increased desire to sleep that accompany mild infections such as colds or "the flu." Accompanying these ideas are those suggesting that the lack of sleep increases susceptibility to infectious disease (Opp and Toth 2003). Despite these widespread beliefs there is little empirical evidence to support the hypotheses that increased sleep aids recovery from, and lack of sleep increases susceptibility to, infections. However, there are data now available addressing the possible molecular regulation of the interactions between infection and altered sleep behavior. Amongst the changes observed are evidence for a cytokine cascade within the brain, including interleukin (IL)-1 and tumor necrosis factor (TNF)-a, along with a number of other substances including growth hormone-releasing hormone (GHRH), prolactin (PL), nitric oxide (NO) and nuclear factor kappa B (NF-kB). These substances, as we shall see below, are also implicated in the regulation of normal spontaneous sleep. The review that follows will focus on altered cytokine production as being of primary importance in sleep physiology in health and disease, but will also pay attention to the role of disruptions in these processes during normal human aging, and its effect on human health.

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