Interleukin-1 β and muramyl dipeptide can prevent decreased antibody response associated with sleep deprivation

Brown, Richard A.; Price, Rhelma J.; King, Maurice G.; Husband, Alan J.

doi:10.1016/0889-1591(89)90031-7

Cited by 46 publications

(16 citation statements)

References 25 publications

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“…In mouse models, short-term sleep deprivation of 6 -14 h has resulted in suppression (reviewed in Ref. 7), no change (61), and enhancement (53, 54) of anti-viral antibody titers.…”

Section: Discussionmentioning

confidence: 99%

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

Everson¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

114

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The specific systems and mechanisms affected by sleep deprivation that may perpetuate disease processes in humans still are speculative. In laboratory rats, prolonged sleep deprivation induces a state marked by abnormal control over indigenous bacteria that results in transient infections of internal tissues and eventual lethal septicemia. The present studies investigated changes in blood, serum, and bone marrow parameters that may provide diagnostic clues to immunopathology. Prolonged sleep deprivation was produced in rats by the disk-over-water method, a well-established and selective means that does not interfere with normal waking behaviors. Measurements included bone and blood differential white blood cell counts, multiple serum cytokines and chemokines, several major Ig classes and subclasses, and serum endotoxin concentrations. The results indicated mild, regenerative neutrophilia in sleep-deprived rats, initially accompanied by immature neutrophils and later by monocytosis. The corresponding serum cytokine profile revealed an evolving proinflammatory state, particularly by high incidence of interleukin-1beta, implicating mononuclear phagocytes and resident tissue cells as main intermediary sources. In addition, multiple serum Ig classes were increased by sleep deprivation without experimental administration of an exogenous antigen. Despite this immune activation, there was failure to eradicate invading bacteria and toxins, suggesting competing anti-inflammatory processes or interference with immune effector functions during sleep deprivation. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as etiological or provocative factors in other disease processes and may provide means by which sleep deprivation as a risk factor in disease may become understood.

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“…In mouse models, short-term sleep deprivation of 6 -14 h has resulted in suppression (reviewed in Ref. 7), no change (61), and enhancement (53, 54) of anti-viral antibody titers.…”

Section: Discussionmentioning

confidence: 99%

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

Everson¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

114

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“…One study using rabbits also reports that sleep deprivation does not exacerbate illness associated with Escherichia coli challenge [57] . Despite these negative data, there are many reports that acute sleep deprivation alters immune functions, including natural killer (NK) cell activity [40,[58][59][60][61] , antigen uptake [62] , phagocytosis [63] , mitogen responses [40,59] , circulating immune complexes [40,64] , circulating IgG levels [65] , secondary antibody responses [66] , the numbers of circulating T cell subsets [61] and cytokine production [10,40,59,63,[67][68][69] .…”

Section: Sleep and Immune Functionsmentioning

confidence: 99%

Bidirectional Communication between the Brain and the Immune System: Implications for Physiological Sleep and Disorders with Disrupted Sleep

Lorton¹,

Lubahn²,

Estus³

et al. 2006

Neuroimmunomodulation

127

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This review describes mechanisms of immune-to-brain and brain-to-immune signaling involved in mediating physiological sleep and altered sleep with disease. The central nervous system (CNS) modulates immune function by signaling target cells of the immune system through autonomic and neuroendocrine pathways. Neurotransmitters and hormones produced and released by these pathways interact with immune cells to alter immune functions, including cytokine production. Cytokines produced by cells of the immune and nervous systems regulate sleep. Cytokines released by immune cells, particularly interleukin-1β and tumor necrosis factor-α, signal neuroendocrine, autonomic, limbic and cortical areas of the CNS to affect neural activity and modify behaviors (including sleep), hormone release and autonomic function. In this manner, immune cells function as a sense organ, informing the CNS of peripheral events related to infection and injury. Equally important, homeostatic mechanisms, involving all levels of the neuroaxis, are needed, not only to turn off the immune response after a pathogen is cleared or tissue repair is completed, but also to restore and regulate natural diurnal fluctuations in cytokine production and sleep. The immune system’s ability to affect behavior has important implications for understanding normal and pathological sleep. Sleep disorders are commonly associated with chronic inflammatory diseases and chronic age- or stress-related disorders. The best studied are rheumatoid arthritis, fibromyalgia and chronic fatigue syndromes. This article reviews our current understanding of neuroimmune interactions in normal sleep and sleep deprivation, and the influence of these interactions on selected disorders characterized by pathological sleep.

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“…Cells were maintained in a RPMI 1640 medium enriched with 10% FCS (Gibco) (inactivated 1 h in a 56°C water bath) and 100 U/ml ofpenicillin (Gibco), 100 Mg/ml ofstreptomycin (Gibco) and 0.29 mg/ml of L-glutamine (Gibco). TC were washed twice with the media and resuspended in 1 ml, after which they were incubated with 0.5 ml of Na25"CrO4 (5 (16). 500 M1 of PBMC (1 X 106 cells/ml) were incubated with 500 ,l ofPHA (1 ul/ml) for 22, 46, and 70 h, and with 500 Ml of RPMI medium (prepared as described above) for 0 and 70 h. After incubation at 37°C and 5% C02, the supernatants were aspirated, leaving the cell pellets.…”

Section: In Vitro Assaysmentioning

confidence: 99%

“…Although sleep changes often accompany fever and systemic infection, including HIV infection (3), there are few experimental data on immune alterations from sleep deprivation. Limited studies in mice (4) and rats (5,6) have failed to document consistent alterations ofimmune responses during sleep loss, although death occurred in rats deprived of sleep for 7-32 d (6).…”

Section: Introductionmentioning

confidence: 99%

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

Dinges

Douglas²,

Zaugg³

et al. 1994

J. Clin. Invest.

321

230

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The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase ofthe cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep. (J. Clin.

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Interleukin-1 β and muramyl dipeptide can prevent decreased antibody response associated with sleep deprivation

Cited by 46 publications

References 25 publications

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

Bidirectional Communication between the Brain and the Immune System: Implications for Physiological Sleep and Disorders with Disrupted Sleep

Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.

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