br Materials and methods br Results br Discussion

Materials and methods
Results
Discussion The results support our hypothesis that the pro/anti-inflammatory complement components can predict PSG sleep measures. The associations between objective sleep measures and inflammatory complement components are similar to those between objective sleep measures and inflammatory cytokines. The majority of the selected PSG sleep measures (66.67%) were predicted by inflammatory complement components and other inflammatory mediators. These results reaffirm the conclusions of previous studies of the existence of an association between objective sleep measures and inflammatory mediators [21–24]. Our results concur with a previous study in healthy individuals that has shown that the inflammatory molecules IL-6 and sICAM-1 are not associated with SOL [21]. Our results extended this study, showing that inflammatory cytokine IL-6, inflammatory cell adhesion molecule sICAM-1 and inflammatory complement components were not associated with SOL (Table 3). Lower sleep duration (TST) was associated with higher sICAM-1, C1INH, CFI and lower C-3. C-3 and sICAM-1 have pro-inflammatory functions [25,26]. C1INH, Factor-H and CFI are anti-inflammatory in nature [3,27]. Lower sleep duration is associated with increased serum inflammatory marker TNF-α [23]. Patel et al. have found that reduced PSG sleep duration is associated with increased levels of pro-inflammatory cytokine TNF-α. The authors concluded that extremes of sleep duration are associated with inflammation [23]. Moreover, similarly to earlier reports [28–30], in this male-exclusive study, no association between sleep duration and IL-6 was found. In CGP 41251 to earlier reports, we did not find an association between IL-6 and REMOL (Table 3) [21,22]. The samples in previous studies included hypertensive individuals, which may have confounded the results because hypertension is associated with IL-6 [31]. Similarly to earlier reports, our study did not find an association between N1 (%) and IL-6 [21,22]. However, N1 (%) was negatively associated with anti-inflammatory complement component Factor-H (Table 3). Both C-3 and C-4 were significantly associated with REM sleep (Table 3). This result is striking, given that there is commonality between the rhythm pattern of C-3, C-4, and REM sleep regulation. REM sleep has a predominant circadian regulation [32], and the serum levels of both C-3 and C-4 have well-characterized circadian patterns [14], which gives further insight into the possible physiological basis of our experimental hypothesis, i.e., the similarity between the association pattern of sleep and inflammatory cytokines and the association pattern of sleep and inflammatory complement components. The circadian aspect of sleep maintains stable and healthy cytokine rhythms [33] and may play a role in the maintenance of stable and healthy complement component rhythms. SWS was positively associated with anti-inflammatory serum complements (C1INH and CFI) and was negatively associated with pro-inflammatory serum C-4 (Table 3), which is in agreement with the theme that poor sleep is associated with increased pro-inflammatory markers and suppressed anti-inflammatory serum cytokine levels [34]. Awake time comprises SOL and WASO and is a negative indicator of sleep quality. In contrast to the report of Taheri et al., 2004, a negative curvilinear relationship between TST and BMI was found (Table 3), which might be due to differences between the samples of the two studies, such as age (almost 3 decades), BMI (approximately 6kg/m2), gender composition, and the presence of chronic diseases, e.g., diabetes and hypertension [24]. The relationship between sleep and inflammatory cytokines is affected by gender [11,35]. Likewise, disease linked differences in sleep and inflammatory cytokines relationship have been previously documented [11]. The findings of this study provide primary evidence of polysomnographic correlates of inflammatory complement components in healthy young males. Future studies should explore the dynamics of this association between objective sleep measures and inflammatory complement components among females and across different age groups and co-morbidities.