Stressor exposure and immunological response in man: Interferon-producing capacity and phagocytosis

Palmblad, Jan; Cantell, Kari; Strander, Hans; Fröberg, Jan; Karlsson, Claes-Göran; Levi, Lennart; Granström, Marta; Unger, Peter

doi:10.1016/0022-3999(76)90020-9

Cited by 150 publications

(62 citation statements)

References 15 publications

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“…In non-sleep-deprived humans, cytokines can be difficult to detect in plasma (34), but there is evidence of them in plasma during sleep deprivation. Palmblad et al (7) found increased IFN production during and after 77 h of sleep loss. Moldofsky et al (9) found that 40 h of sleep deprivation enhanced IL-1-like and IL-2-like activities.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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

View full text Add to dashboard Cite

show abstract

“…This does not, however, account for the lower viral titers observed in the nasal secretions of the sleep deprived animals. Palmblad et al 12 reported that interferon levels are increased in the tracheal washes of sleep-deprived soldiers undergoing night patrols, presumably due to enhancement of the interferon-producing capacity of lymphocytes. Since interferon prevents productive infection of cells by influenza virus, 13 an increase in this cytokine could explain our results.…”

Section: Discussionmentioning

confidence: 99%

REM Sleep and Mood State in Childbearing Women: Sleepy or Weepy?

Lee

McEnany

Zaffke

2000

Sleep

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“…Sleep loss enhances lymphocyte IFN production [63] , increases white blood cell and monocyte TNF production [71] , elevates cultured whole blood cell production of IL-1 ␤ and IFN-␣ [67] and raises plasma IL-1 activity in humans and rats [40,68] . In addition, plasma TNF levels are altered in obstructive sleep apnea syndrome patients [44] .…”

Section: Sleep and Immune Functionsmentioning

confidence: 99%

“…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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Stressor exposure and immunological response in man: Interferon-producing capacity and phagocytosis

Cited by 150 publications

References 15 publications

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

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

REM Sleep and Mood State in Childbearing Women: Sleepy or Weepy?

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

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