The Rationale for Studying Sleep and Immunity in Clinical Populations

Substantial evidence demonstrates that sleep and the immune system interact via bidirectional pathways (Krueger et al. 1995; Opp 2005). Experimental strategies that target sleep (e.g., sleep deprivation) or modify the immune system (via the cytokine network) are beginning to identify the mechanisms that link sleep and immunity. Basic studies show that inflammatory cytokine administration alters sleep macroarchitecture and continuity (Spath-Schwalbe et al. 1998; Spath-Schwalbe, Lange, Perras, Fehm, and Born 2000; Hogan, Morrow, Smith, and Opp 2003). Conversely, sleep behavior influences immunity; with as few as 4 h of sleep loss altering lymphocyte trafficking, cytokine expression, and effector cell activity (Motivala and Irwin 2005); furthermore, prolonged sleep deprivation in rats (>2 weeks) results in death due to poor host defense of normally controlled bacterial pathogens that progressively penetrate into multiple organ systems (Everson and Toth 2000). These studies suggest that chronic sleep impairments show a reciprocal relationship with immune dysregulation. There is growing interest in testing the impact of chronic loss of sleep on the immune system in clinical disorders in which there are marked sleep impairments. Such studies have the potential to provide insights into the reciprocal influence of cytokines on sleep, and whether increases in inflammatory markers in many of these disorders might contribute to abnormalities in sleep continuity or sleep depth in these populations. In addition, immune dysregulation due to sleep impairments may impact the incidence of infectious diseases and the development of inflammatory disorders in these vulnerable populations. This chapter focuses on these clinical populations who have disordered sleep and/or inflammation and examines the hypothesis that sleep impairments initiate increased expression of inflammatory cytokines that are part of a positive feedback loop that promotes and perpetuates sleep impairments and low-grade inflammatory processes.

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