OSAS Neuroimmunology

The links between immune system and sleep were first identified in the 1970s, when a sleep-inducing factor was isolated and chemically characterized from human urine: Factor S, a muramyl peptide derived from bacterial peptoglycan. Subsequently muramyl dipeptide and Factor S-related peptidoglycans were all shown to induce the key immunoregulatory cytokine. Then interleukin (IL)-ip was shown to be a potent somnogen, as well as a potent pyrogen. In fact, IL-ip is one of the most neurologically active molecules known. Subsequent studies revealed that bacterial LPS, LPS components, and viral synthetic dsRNA, as well as killed and living bacteria can induce IL-1, tumor necrosis factor (TNF)-a, IL-6, and IL-10 (Majde and

Krueger 2005). The presence of systemic inflammation, characterized by an elevation of certain potent proinflammatory cytokines, such as IL-1, IL-6, IL-10, and TNF-a may predispose patients with OSAS to develop cardiovascular complications. Alberti, Sarchielli, Gallinella, Floridi, Mazzotta, and Gallai (2003) reported a prevailing activation of the Th1-type cytokine pattern in OSAS patients, which is not associated with the severity and duration of OSAS. A factor critical for the development of an effective immune response is the cytokine balance between T helper (Th1) and T helper 2 (Th2) cells, determining the selection of the effector mechanisms of type 1 or type 2 immunity. Th1 cells releasing mainly interferon-y (INF-y), aside from other cytokines including IL-2 and TNF-a become activated in response to intracellular viral and bacterial challenges and support various cellular (type 1) responses, including macrophage activation and antigen presentation. In contrast, the cytokines characteristic of Th2 immunity, IL-4 as well as IL-5, IL-10, and IL-13 tend to drive humoral (type 2) defense via stimulating mast cells, eosinophils and B cells against extracellular pathogens. Predominance of type 2 cytokines, has been associated with a reduced response to vaccination (Ginaldi et al. 1999) on the other hand (Petrovsky and Harrison 1997) suggest that nocturnal sleep could favor a shift towards Th1 mediate immune defense. They found a circadian peak of the ratio of IFN-y/IL-10 production in whole blood samples during nocturnal sleep. This peak was completely abolished following administration of cortisone acetate al 9:00 p.m. in the preceding evening, suggesting that the suppression of endogenous cortisol release during early sleep plays a mediating role for this Th1 shift. However, SWS not only suppresses the release of glucocorticoids but also promotes the release of growth hormone (GH) and prolactin, which appears to support Th1-cell-mediated immunity (Chikanza and Dimitrov 1999).

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