Systemic bacterial invasion induced by sleep deprivation

Everson, Carol A.; Toth, Linda A

doi:10.1152/ajpregu.2000.278.4.r905

Cited by 183 publications

(177 citation statements)

References 39 publications

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“…Hence, the suppressing effects of acute experimental sleep loss on immunological memory formation observed in the current study seem to apply also to natural variations in sleep, underscoring the clinical relevance of our findings. Prolonged experimental sleep restriction likewise consistently revealed a negative impact on immune functions (7,49). However, as habitual short sleep and experimental sleep restriction may not always lead to reduced SWS or SWA (50,51), such immunosuppressive effects may stem rather from more pronounced endocrine changes like overall increases in cortisol levels (8).…”

Section: Discussionmentioning

confidence: 99%

Sleep after Vaccination Boosts Immunological Memory

Lange

Dimitrov

Bollinger

et al. 2011

The Journal of Immunology

152

146

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Sleep regulates immune functions. We asked whether sleep can influence immunological memory formation. Twenty-seven healthy men were vaccinated against hepatitis A three times, at weeks 0, 8, and 16 with conditions of sleep versus wakefulness in the following night. Sleep was recorded polysomnographically, and hormone levels were assessed throughout the night. Vaccination-induced Th cell and Ab responses were repeatedly monitored for 1 y. Compared with the wake condition, sleep after vaccination doubled the frequency of Ag-specific Th cells and increased the fraction of Th1 cytokine-producing cells in this population. Moreover, sleep markedly increased Ag-specific IgG1. The effects were followed up for 1 y and were associated with high sleep slow-wave activity during the postvaccination night as well as with accompanying levels of immunoregulatory hormones (i.e., increased growth hormone and prolactin but decreased cortisol release). Our findings provide novel evidence that sleep promotes human Th1 immune responses, implicating a critical role for slow-wave sleep in this process. The proinflammatory milieu induced during this sleep stage apparently acts as adjuvant that facilitates the transfer of antigenic information from APCs to Ag-specific Th cells. Like the nervous system, the immune system takes advantage of the offline conditions during sleep to foster adaptive immune responses resulting in improved immunological memory.

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Section: Discussionmentioning

confidence: 99%

Sleep after Vaccination Boosts Immunological Memory

Lange

Dimitrov

Bollinger

et al. 2011

The Journal of Immunology

152

146

View full text Add to dashboard Cite

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“…Notably, the human studies were performed mainly on depressive patients, and it is doubtful whether these can be regarded as a representative group of the whole population. In animal experiments, after 72 hours of sleep loss, the level of the corticotropin-releasing hormone (CRH) changed the absence of the nocturnal maximal GH release in the sleep-deprived animals [72,73], or to a tendency for such animals to become infected with their own migrating bacterial flora [74]. These conjectures are in contradiction with the findings indicating that REM loss does not disrupt the wound healing process [75].…”

Section: Dermal Effectsmentioning

confidence: 92%

“…However, even the authors themselves have found this outcome surprising. The sleep-deprived animals develop infections of the lymph glands and other tissues, which are induced by their own intestinal bacterial flora [74]. This can take place only in the state of immunological suppression.…”

Section: Dermal Effectsmentioning

confidence: 99%

Consequences of sleep deprivation

Orzeł-Gryglewska¹

2010

International Journal of Occupational Medicine and Environmental Health

211

133

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This paper presents the history of research and the results of recent studies on the effects of sleep deprivation in animals and humans. Humans can bear several days of continuous sleeplessness, experiencing deterioration in wellbeing and effectiveness; however, also a shorter reduction in the sleep time may lead to deteriorated functioning. Sleeplessness accounts for impaired perception, difficulties in keeping concentration, vision disturbances, slower reactions, as well as the appearance of microepisodes of sleep during wakefulness which lead to lower capabilities and efficiency of task performance and to increased number of errors. Sleep deprivation results in poor memorizing, schematic thinking, which yields wrong decisions, and emotional disturbances such as deteriorated interpersonal responses and increased aggressiveness. The symptoms are accompanied by brain tissue hypometabolism, particularly in the thalamus, prefrontal, frontal and occipital cortex and motor speech centres. Sleep deficiency intensifies muscle tonus and coexisting tremor, speech performance becomes monotonous and unclear, and sensitivity to pain is higher. Sleeplessness also relates to the changes in the immune response and the pattern of hormonal secretion, of the growth hormone in particular. The risk of obesity, diabetes and cardiovascular disease increases. The impairment of performance which is caused by 20-25 hours of sleeplessness is comparable to that after ethanol intoxication at the level of 0.10% blood alcohol concentration. The consequences of chronic sleep reduction or a shallow sleep repeated for several days tend to accumulate and resemble the effects of acute sleep deprivation lasting several dozen hours. At work, such effects hinder proper performance of many essential tasks and in extreme situations (machine operation or vehicle driving), sleep loss may be hazardous to the worker and his/her environment.

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“…83). Already well established is the fact that acutely sustained total sleep deprivation in laboratory rats results in a progressive negative energy balance (2, 20, 28), suppression of major anabolic hormones (21, 24), and immune-related abnormalities (18,19,26,27) that turn lethal after an average of 16 to 21 days (20,53,55,62). However, rats that obtain nearly half-normal sleep amounts during the same time period do not develop severe pathology and do not die (20,53,55,62).…”

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confidence: 99%

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

Everson¹,

Szabó

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Everson CA, Szabo A. Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes. Am J Physiol Regul Integr Comp Physiol 297: R1430-R1440, 2009. First published August 19, 2009 doi:10.1152/ajpregu.00230.2009.-Chronic restriction of a basic biological need induces adaptations to help meet requisites for survival. The adaptations to chronic restriction of sleep are unknown. A single episode of 10 days of partial sleep loss in rats previously was shown to be tolerated and to result in increased food intake and loss of body weight as principal signs. The purpose of the present experiment was to investigate the extent to which adaptation to chronic sleep restriction would ameliorate short-term effects and result in a changed internal phenotype. Rats were studied during 10 wk of multiple periods of restricted and unrestricted sleep to allow adaptive changes to develop. Control rats received the same ambulatory requirements only consolidated into periods that lessened interruptions of their sleep. The results indicate a latent period of relatively stable food and water intake without weight gain, followed by a dynamic phase marked by enormous increases in food and water intake and progressive loss of body weight, without malabsorption of calories. Severe consequences ensued, marked especially by changes to the connective tissues, and became fatal for two individuals. The most striking changes to internal organs in sleep-restricted rats included lengthening of the small intestine, decreased size of adipocytes, and increased incidence of multilocular adipocytes. Major organs accounted for an increased proportion of total body mass. These changes to internal tissues appear adaptive in response to high energy production, decomposition of lipids, and increased need to absorb nutrients, but ultimately insufficient to compensate for inadequate sleep. sleep rebound; adaptation; metabolism; adiposity; connective tissues; visceral organs CHRONIC DEFICIENCIES IN BASIC biological requirements produce disease. This basic principle has been well established for nutrition, hydration, and oxygen. It also is believed to be true for sleep. However, the specific physiological properties and outcomes of chronic sleep deficiency are not well elucidated. Most studies on the effects of inadequate sleep have employed previously well-rested, young, normal human and animal subjects under conditions of acute and short-term sleep loss. As may be expected, early physical signs of deprivation seem nonspecific, while subject complaints and poor cognitive performance are pronounced (e.g., reviewed in Refs. 7, 38, 48, and 52). Recently, findings in humans undergoing sleep restriction prolonged for six nights suggest sleep loss produces risk factors for obesity, diabetes, and hypertension (45, 71), but questions arise about the extent to which outcomes can be extrapolated to conditions of chronic deficiency and actually become realized. Epidemiological studies show strong linkages between sleep los...

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Systemic bacterial invasion induced by sleep deprivation

Cited by 183 publications

References 39 publications

Sleep after Vaccination Boosts Immunological Memory

Sleep after Vaccination Boosts Immunological Memory

Consequences of sleep deprivation

Recurrent restriction of sleep and inadequate recuperation induce both adaptive changes and pathological outcomes

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