Effects of sleep and circadian rhythm on the human immune system: Annals of the New York Academy of Sciences

Department of Neuroendocrinology, University of Lübeck, Lübeck, Germany.
Annals of the New York Academy of Sciences (Impact Factor: 4.38). 04/2010; 1193(1):48-59. DOI: 10.1111/j.1749-6632.2009.05300.x
Source: PubMed


Many immune parameters show systematic fluctuations over the 24-h day in human blood. Circulating naive T-cells and production of proinflammatory cytokines, like interleukin-12 (IL-12), peak during nighttime, whereas cytotoxic effector leukocytes and production of the anti-inflammatory cytokine IL-10 peak during daytime. These temporal changes originate from a combined influence of the circadian system and sleep. Both brain functions act synergistically and share neuroendocrine effector mechanisms to convey control over immune functions. Sympathetic tone and cortisol levels show a circadian nadir during nighttime and are further suppressed by sleep, whereas growth hormone and prolactin show a circadian peak during nighttime and are further enhanced by sleep. Thus, the circadian system and sleep jointly evoke a unique endocrine constellation that is extremely effective in inducing changes in leukocyte traffic and a shift toward proinflammatory type 1-cytokines during the nocturnal period of sleep, that is, an action with strong clinical implications.

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    • "On the level of neural systems, an functional magnetic resonance imaging (fMRI) study of the development of statistical knowledge suggested that a hippocampaleneocortical transfer occurs during the period of sleep and that weaker parahippocampal responses occur following sleep than following wakefulness [98]. Although the complementary systems model has mostly been studied in terms of declarative memory, this model may also apply to memory formation in other systems and has even been used to explain immunological memory formation [99]. "

    • "Lack of sleep is associated with higher risk of suffering from infections and worse recovery, and with increased risk of developing non-infectious diseases and chronic low-grade inflammation [5]. These conditions are linked to alterations in the immune response, which may be secondary to the activation of the stress axis and the release of cortisol, a well-known regulator of immune activity; however, it cannot be ruled out that changes in immune parameters respond to a direct crosstalk between sleep and the immune system [6]–[8]. "
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    ABSTRACT: Background Sleep patterns face important changes during adolescence. This can have implications for the immune system, which is regulated by the sleep–wake cycle; however, most studies relating sleep and immune system have been conducted on adults. Objective To study the relationships between sleep duration, immune cell counts and cytokines in European adolescents participating in the HELENA Cross-Sectional Study. Methods Adolescents (12.5–17.5 years; n = 933; 53.9% girls) were grouped according to self-reported sleep duration into <8, 8–8.9 and ≥9 h/night. Blood samples were collected in the morning after an overnight fast to analyze counts of white blood cells (WBC), neutrophils, lymphocytes, monocytes, eosinophils, basophils, the lymphocyte subsets CD3+, CD4+, CD8+, CD45RA+, CD45RO+, CD3−CD16+56+ and CD19+, and concentrations of cortisol, CRP, IL-1, IL-2, IL-4, IL-5, IL-6, IL-10, TNF-α and IFN-γ. Pro-/anti-inflammatory and Th1/Th2 cytokine ratios were calculated. Immune parameters were correlated to sleep duration and compared between the three groups. Results Sleep duration was negatively associated with cortisol levels and WBC, neutrophil, monocyte, CD4+ and CD4+CD45RO+ counts, and in girls also with IL-5 and IL-6 levels. The 8–8.9 h/night group presented the highest IL-4 values and the lowest pro-/anti-inflammatory and Th1/Th2 cytokine ratios. Conclusion A sleep duration of 8–8.9 h/night was associated with a healthier immune profile in our adolescents.
    Sleep Medicine 10/2014; 15(10). DOI:10.1016/j.sleep.2014.04.010 · 3.15 Impact Factor
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    • "Several parameters have been used to analyze the immune-neuroendocrine relations, in both nonspecific and specific immunity and, within this, both cell and humoral response [52–55]. "
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    ABSTRACT: The aging process involves a decline in immune functioning that renders elderly people more vulnerable to disease. In residential programs for the aged, it is vital to diminish their risk of disease, promote their independence, and augment their psychological well-being and quality of life. We performed a randomized controlled study, evaluating the ability of a relaxation technique based on Benson’s relaxation response to enhance psychological well-being and modulate the immune parameters of elderly people living in a geriatric residence when compared to a waitlist control group. The study included a 2-week intervention period and a 3-month follow-up period. The main outcome variables were psychological well-being and quality of life, biomedical variables, immune changes from the pre-treatment to post-treatment and follow-up periods. Our findings reveal significant differences between the experimental and control groups in CD19, CD71, CD97, CD134, and CD137 lymphocyte subpopulations at the end of treatment. Furthermore, there was a decrease in negative affect, psychological discomfort, and symptom perception in the treatment group, which increased participants’ quality of life scores at the three-month follow-up. This study represents a first approach to the application of a passive relaxation technique in residential programs for the elderly. The method appears to be effective in enhancing psychological well-being and modulating immune activity in a group of elderly people. This relaxation technique could be considered an option for achieving health benefits with a low cost for residential programs, but further studies using this technique in larger samples of older people are needed to confirm the trends observed in the present study. Trial registration International Standard Randomised Controlled Trial Number Register ISRCTN85410212
    BMC Complementary and Alternative Medicine 08/2014; 14(1):311. DOI:10.1186/1472-6882-14-311 · 2.02 Impact Factor
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