Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Abstract

Background/Aims: Several lines of evidence indicate that sleep loss imposes significant consequences on the host defense system, including changes in cell number, activity and distribution. However, it is not clear whether cellular alterations after sleep deprivation are caused by redistribution to immune organs or by death of these cells or how the response to a nonspecific immune activator would be affected. Therefore, the aim of this study was to assess the leukocyte distribution after paradoxical sleep deprivation (PSD) in saline- and lipopolysaccharide-treated mice. Methods: Adult inbred mice were paradoxical sleep deprived (72 h), whereas the controls were kept in their home cages. After PSD, both groups received an injection of either saline or lipopolysaccharide (LPS; 1 or 5 µg/animal, intraperitoneally), 2 h prior to the collection of blood, spleen, lymph nodes and peritoneal wash. Isolated cells were then designated to differential leukocyte count (blood) and flow cytometry analysis of immune cell subsets (immune sites). Results: The data revealed that PSD caused a significant reduction of circulating lymphocytes and a general decrease in all cellular subsets of spleen, mainly T and B cells. However, no alteration in response of PSD was found on other immune sites, such as lymph nodes and peritoneum. Of note, immune cell distribution in response to in vivo LPS stimulation remained unchanged after PSD. Conclusions: Our study provided original evidence concerning the immune outcomes of PSD, indicating that cellular decrease caused by PSD is not restricted to circulation, but also to immune sites. Taken together, our results could help shed light on the physiological mechanisms of leukocyte trafficking.

Sleep Loss and Cytokines Levels in an Experimental Model of Psoriasis

“…Pruritus, depression, and pain interfere with sleep duration and structure by increasing nocturnal awakenings and leading to sleep deprivation and fragmentation [17]. Lack of sleep itself has important effects on immunological integrity and nocturnal secretion of cytokines [18], [19], [20], [21], [22], [23], [24] and may be considered another risk factor for psoriasis. This bi-directional interaction between the central nervous system and the immune system has been focus of intense research in recent decades [25].…”

Sleep deprivation attenuates endotoxin-induced cytokine gene expression independent of day length and circulating cortisol in male Siberian hamsters (Phodopus sungorus)

“…bees (Beyaert et al, 2012), songbirds (Jones et al, 2010), rodents (Zager et al, 2007;Zager et al, 2012)]. A growing body of experimental and epidemiological studies has demonstrated that sleep loss induces alterations in the immune system that predispose individuals towards disease (Faraut et al, 2012).…”

“…Even a single night of partial sleep loss can induce a rapid increase in nuclear-factor-kappa B activity, the transcription factor that promotes pro-inflammatory gene expression (Irwin et al, 2008;Irwin et al, 2010). Alternatively, during an infection or inflammatory challenge, such as bacterial lipopolysaccharide (LPS) exposure, sleep deprivation attenuates cellular immunity (Zager et al, 2012), alters sickness behavior (Zager et al, 2009) and suppresses pro-inflammatory mRNA expression in the periphery and brain (Weil et al, 2009). A common feature of sleep loss is activation of the hypothalamic-pituitaryadrenal axis (Meerlo et al, 2002), which leads to a moderate and transient elevation in circulating glucocorticoids.…”

Chronic Sleep Restriction Impairs the Antitumor Immune Response in Mice

“…The literature indicates that SD modifies the profile of circulating leukocytes and the production of cytokines in human and animal models, with or without immunological challenge [31][32][33][34][35][36]. Moreover, it is also well described that stress hormones prevent the migration and activation of leukocytes [37].…”