Sleep–Immune System Interaction: Advantages and Challenges of Human Sleep Loss Model

Md Dilshad Manzar,M Ejaz Hussain

doi:10.3389/fneur.2012.00002

Abstract

Sleep and its functional interaction with immune system is well recognized (Majde and Krueger, 2005; Krueger and Majde, 2011). Sleep synchronized changes in brain activity are implicated in direct rather than indirect immune function (Bryant et al., 2004). Sleep or at least its homeostatic component has been suggested to have an active auto-regulatory and/or auto-modulatory mechanism (Krueger et al., 2008; Kumar, 2010). This mechanism operates through adenosine and other sleep regulating substances (SRSs) like interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), growth-hormone-releasing hormone (GHRH), corticotropin-releasing hormone (CRH), nitric oxide (NO), prostaglandin D2 (PGD2), etc. These SRSs are most likely the connecting link between sleep and immune system (Krueger et al., 2008). The issue of peripheral cytokines affecting brain signaling in sleep has been reviewed comprehensively with three suggested routes for transfer of peripheral cytokines to the brain (Krueger and Majde, 2003). These routes may also be involved in transfer and hence in transmitting the signals from peripheral SRSs. Sleep–immune system co-relations has been investigated across a wide range of immune parameters out of which cytokines, immune cells, antibodies, and neuro-endocrine system constitute the focal group. Human sleep loss (SL) models have been of great help in mechanistic characterization of cytokines (IL-1β and TNF-α role) in sleep and neuroendocrine components (GHRH and CRH) in non-REM sleep, respectively (Majde and Krueger, 2005; Krueger and Majde, 2011). The paradigm has helped establish sleep's functional characterization because of practical simplicity (Reynolds and Banks, 2010) and often non-ambiguous results. However, there may be certain limitations with SL model in context of result translation pertaining to different parameter patterns. The comment has been surmised to highlight these challenges which may give direction to future research in minimizing the variable factors. It may also help to compare the results from available literature objectively.

Highlights

Sleep and its functional interaction with immune system is well recognized (Majde and Krueger, 2005; Krueger and Majde, 2011)
STNFR p55 level did not alter on partial sleep deprivation (PSD) (Haack et al, 2007; Boudjeltia et al, 2008) but it increased on three nights of total sleep deprivation (TSD) (Haack et al, 2007)
The co-relationship between stress and blood pressure (Gasperin et al, 2009) and increase in blood pressure on TSD with different sleep loss (SL) designs has been reported by three studies (Meier-Ewert et al, 2004)

Summary

Introduction

Sleep and its functional interaction with immune system is well recognized (Majde and Krueger, 2005; Krueger and Majde, 2011). TSD (both acute and chronic variations) and PSD have been used widely, sleep disruption has been very rarely employed (Reynolds and Banks, 2010). STNFR p55 level did not alter on PSD (Haack et al, 2007; Boudjeltia et al, 2008) but it increased on three nights of TSD (Haack et al, 2007).

Results

Conclusion