Differential Effects of Rapid Eye Movement Sleep Deprivation and Immobilization Stress on Blood Lymphocyte Subsets in Rats

Velázquez‐Moctezuma, Javier; Domı́nguez-Salazar, Emilio; Cortés-Barberena, Edith; Nájera-Medina, Oralia; Retana‐Márquez, Socorro; Rodriguez-Aguilera, Ernesto; Jiménez-Anguiano, Anabel; Cortes-Martinez, Leticia; Ortiz-Muñiz, Rocío

doi:10.1159/000078445

Cited by 22 publications

(14 citation statements)

References 38 publications

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“…Regarding the general reduction of immune cell populations in saline-treated mice, these data are in accordance with previous findings showing decreased circulating lymphocyte populations after PSD in humans [25,26] and rodents [17,18,27] . The current study expanded our previous findings [18] by demonstrating that this reduction occurs not only in circulating lymphocytes but also in spleen and in other cell subtypes, such as macrophages, NK cells and dendritic cells.…”

Section: Discussionsupporting

confidence: 92%

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Zager

Ruiz

Tufik

et al. 2012

Neuroimmunomodulation

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Background/Aims: Several lines of evidence indicate that sleep loss imposes significant consequences on the host defense system, including changes in cell number, activity and distribution. However, it is not clear whether cellular alterations after sleep deprivation are caused by redistribution to immune organs or by death of these cells or how the response to a nonspecific immune activator would be affected. Therefore, the aim of this study was to assess the leukocyte distribution after paradoxical sleep deprivation (PSD) in saline- and lipopolysaccharide-treated mice. Methods: Adult inbred mice were paradoxical sleep deprived (72 h), whereas the controls were kept in their home cages. After PSD, both groups received an injection of either saline or lipopolysaccharide (LPS; 1 or 5 µg/animal, intraperitoneally), 2 h prior to the collection of blood, spleen, lymph nodes and peritoneal wash. Isolated cells were then designated to differential leukocyte count (blood) and flow cytometry analysis of immune cell subsets (immune sites). Results: The data revealed that PSD caused a significant reduction of circulating lymphocytes and a general decrease in all cellular subsets of spleen, mainly T and B cells. However, no alteration in response of PSD was found on other immune sites, such as lymph nodes and peritoneum. Of note, immune cell distribution in response to in vivo LPS stimulation remained unchanged after PSD. Conclusions: Our study provided original evidence concerning the immune outcomes of PSD, indicating that cellular decrease caused by PSD is not restricted to circulation, but also to immune sites. Taken together, our results could help shed light on the physiological mechanisms of leukocyte trafficking.

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Section: Discussionsupporting

confidence: 92%

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Zager

Ruiz

Tufik

et al. 2012

Neuroimmunomodulation

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“…Overall, both TAIEP and SD rats are associated with an increase in the populations of B cells (CD45+) and NK cells (NK1.1+) in the spleen, and stress is also associated with increased total T cells (CD3+), but in contrast, the SD condition is associated with a decrease in the cytotoxic T cell subpopulation (CD8+CD3+). These results are in agreement with those from Velazquez-Moctezuma, 2004, which reported similar changes with different stressors, and therefore, we can postulate that the overall response of the cell subpopulations depends on the immune system nature of the stressor and the basal condition of the CNS and in this case myelin loss [28]. The major differences of taiep rats in comparison with Sprague-Dawley are that cytokines such as IFN-γ, TNF-α, and were unaltered but IL-1β and IL-10 were downregulated in 1-month-old taiep rats.…”

Section: Discussionsupporting

confidence: 92%

The lack of myelin in the mutanttaieprat induces a differential immune response related to protection to the human parasiteTrichinella spiralis

Nava-Castro

Cortes

Eguíbar

et al. 2020

Preprint

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24Taiep rat is a myelin mutant with a progressive motor syndrome characterized by tremor, 25 ataxia, immobility episodes, epilepsy and paralysis of the hindlimbs, accompanied with differential 26 expression of interleukins and their receptors that correlated with the progressive demyelination that 27 characterize this mutant. Thus, the taiep rat is a suitable model to study neuroimmune alterations.28 The aim of this study was to investigate the immune alterations present in the mutant taiep rat during 29 the acute infection with Trichinella spiralis. Our results show that there is an important decrease in 30 the number of intestinal larvae in the taiep rat when compared to the Sprague-Dawley control rats. 31 We also found differences in the percentage of innate and adaptive immune cell profile in the 32 mesenteric lymphatic nodes and the spleen associated to the lack of myelin in the taiep rat. Finally, a 33 clear pro-inflammatory cytokine pattern was seen in the infected taiep rat, which may explain the 34 decrease in larvae number. These results sustain the theory that neuroimmune interaction is a 35 fundamental process capable of modulating the immune response, particularly against the parasite 36 Trichinella spiralis in a model of progressive demyelination that could be an important mechanism in 37 autoimmune diseases and parasite infection. 39Author summary 40 The complex communication among the brain and the immune system may be certainly 41 altered during an infection and may be determinant in the resolution of this. We analyze the immune 42 response to a parasite in a rat model in which a demyelinization process occur naturally and found 43 that parasite loads were reduced when comparing with control subjects and this was accompanied to 44 changes in the systemic immune response.3 45 Introduction 46The interaction of the nervous, endocrine and immune systems is crucial in the maintenance 47 of homeostasis in vertebrates and it is absolutely vital in mammals [1]. Moreover, hormones and 48 neurotransmitters present in the immune cell microenvironment can restrict their autonomy, probably 49 by acting on receptors of these neuroendocrine factors [2]. Therefore, efficient communication 50 among these three systems implies the existence of afferent and efferent pathways, constituting a 51 complex feedback system that regulates an adequate response in base of different insults. 52Alterations of this network trigger pathologies that involve all the system components. In 53 recent years, information on the multiple functions of the immune system has expanded remarkably;54 one of these functions has been biological adaptation through elimination of pathogens and foreign 55 cells from the organism [3]. All functions require delicate control systems, which will allow 56 adaptation of the organism to different physiological and pathological situations, which will face it a 57 longer life. To meet this end, interaction with nervous and endocrine systems of the organism is 58 necessary [3]. This interaction is const...

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“…described an increase in the number of neutrophils and T lymphocytes after 2 days of total sleep deprivation or 4 days of REM‐sleep deprivation in humans; interestingly, only neutrophils reached basal values after 1 night of sleep recovery, while high numbers of T cells persisted even after 3 nights of sleep recovery. Paradoxically, in a rodent model we found that REM sleep deprivation for 10 days increased the number of NK cells, but decreased the number of T lymphocytes 63 . The reported differences among human studies in the effects of sleep loss on white blood cell counts seem to arise from the length of sleep deprivation and of the age of the participants.…”

Section: Sleep Loss and The Immune Responsementioning

confidence: 59%

Role of sleep in the regulation of the immune system and the pituitary hormones

Gómez-González

Domı́nguez-Salazar

Hurtado‐Alvarado

et al. 2012

Annals of the New York Academy of Sciences

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Sleep is characterized by a reduced response to external stimuli and a particular form of electroencephalographic (EEG) activity. Sleep is divided into two stages: REM sleep, characterized by muscle atonia, rapid eye movements, and EEG activity similar to wakefulness, and non-REM sleep, characterized by slow EEG activity. Around 80% of total sleep time is non-REM. Although it has been intensely studied for decades, the function (or functions) of sleep remains elusive. Sleep is a highly regulated state; some brain regions and several hormones and cytokines participate in sleep regulation. This mini-review focuses on how pituitary hormones and cytokines regulate or affect sleep and how sleep modifies the plasma concentration of hormones as well as cytokines. Also, we review the effects of hypophysectomy and some autoimmune diseases on sleep pattern. Finally, we propose that one of the functions of sleep is to maintain the integrity of the neuro-immune-endocrine system.

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Differential Effects of Rapid Eye Movement Sleep Deprivation and Immobilization Stress on Blood Lymphocyte Subsets in Rats

Cited by 22 publications

References 38 publications

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

Immune Outcomes of Paradoxical Sleep Deprivation on Cellular Distribution in Naive and Lipopolysaccharide-Stimulated Mice

The lack of myelin in the mutanttaieprat induces a differential immune response related to protection to the human parasiteTrichinella spiralis

Role of sleep in the regulation of the immune system and the pituitary hormones

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