Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus

Palma, Beatriz Duarte; Gabriel, Alexandre; Colugnati, Fernando Antônio Basile; Tufik, Sérgio

doi:10.1152/ajpregu.00186.2006

Cited by 60 publications

(50 citation statements)

References 54 publications

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“…Previous data from our laboratory indicated that the NZB/NZWF 1 mice subjected to SD had an earlier onset of the disease as reflected by an increased number of ANA (11). In the present study, we had hypothesized that the SD could increase PRL secretion, and this would be involved in an earlier onset of the disease.…”

Section: Discussionmentioning

confidence: 66%

“…Throughout the study both groups had free access to food and water. This experimental protocol was carried out in an attempt to simulate a chronic condition of SD (similar to that which is observed in chronic inflammatory disease) (11).…”

Section: Sleep Deprivationmentioning

confidence: 99%

“…In addition, the disease is exacerbated by sleep disruption. Recent data from our laboratory indicated that the NZB/ NZWF 1 mice subjected to sleep deprivation (SD) show an earlier onset of the disease reflected by increased numbers of ANA (11). There is evidence to support the view that sleep disturbances lead to hormonal, neurochemical and immunological alterations that may be linked to disease manifestation (12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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Effects on prolactin secretion and binding to dopaminergic receptors in sleep-deprived lupus-prone mice

Palma

Hipólide

Tufik

2009

Braz J Med Biol Res

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Sleep disturbances have far-reaching effects on the neuroendocrine and immune systems and may be linked to disease manifestation. Sleep deprivation can accelerate the onset of lupus in NZB/NZWF 1 mice, an animal model of severe systemic lupus erythematosus. High prolactin (PRL) concentrations are involved in the pathogenesis of systemic lupus erythematosus in human beings, as well as in NZB/NZWF 1 mice. We hypothesized that PRL could be involved in the earlier onset of the disease in sleep-deprived NZB/NZWF 1 mice. We also investigated its binding to dopaminergic receptors, since PRL secretion is mainly controlled by dopamine. Female NZB/NZWF 1 mice aged 9 weeks were deprived of sleep using the multiple platform method. Blood samples were taken for the determination of PRL concentrations and quantitative receptor autoradiography was used to map binding of the tritiated dopaminergic receptor ligands [ 3 H]-SCH23390, [ 3 H]-raclopride and [ 3 H]-WIN35,428 to D 1 and D 2 dopaminergic receptors and dopamine transporter sites throughout the brain, respectively. Sleep deprivation induced a significant decrease in plasma PRL secretion (2.58 ± 0.95 ng/mL) compared with the control group (25.25 ± 9.18 ng/mL). The binding to D 1 and D 2 binding sites was not significantly affected by sleep deprivation; however, dopamine transporter binding was significantly increased in subdivisions of the caudate-putamen -posterior (16.52 ± 0.5 vs 14.44 ± 0.6), dorsolateral (18.84 ± 0.7 vs 15.97 ± 0.7) and ventrolateral (24.99 ± 0.5 vs 22.54 ± 0.7 μCi/g), in the sleep-deprived mice when compared to the control group. These results suggest that PRL is not the main mechanism involved in the earlier onset of the disease observed in sleepdeprived NZB/NZWF 1 mice and the reduction of PRL concentrations after sleep deprivation may be mediated by modifications in the dopamine transporter sites of the caudate-putamen.

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Section: Discussionmentioning

confidence: 66%

Section: Sleep Deprivationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects on prolactin secretion and binding to dopaminergic receptors in sleep-deprived lupus-prone mice

Palma

Hipólide

Tufik

2009

Braz J Med Biol Res

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“…Since MS is considered an immune-mediated disease, the researchers of this study hypothesize that sleep disturbances may facilitate acute relapses via changes in the immune system function. According to a study on an animal model of systemic lupus erythematous, sleep deprivation is associated with an accelerated autoantibody production rate [20]. Sleep disorders also result in elevated serum concentration of interleukin-6 (IL-6) [21], which further activates polyclonal B cells and triggers an auto-immune reaction [22].…”

Section: Discussionmentioning

confidence: 99%

Sleep Disorder as a Triggering Factor for Relapse in Multiple Sclerosis

et al. 2017

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Background/Aims: To determine the effect of sleep disturbances on predisposing multiple sclerosis (MS) patients for acute relapse. Methods: This case-control study was conducted on 80 MS patients including 40 patients in the remission phase and 40 in the relapse phase. Patients were asked to fill in the Pittsburgh Sleep Quality Index to determine their sleep quality during the previous month. Individuals with scores of 5 or less were considered having normal sleep quality. Results: Mean ± SD ages were 32.5 ± 7.7 and 30.2 ± 7.2 years among patients with and without acute relapses, respectively (p > 0.05). The mean disease duration and disease severity (according to Expanded Disability Status Scale [EDSS]) were comparable across the groups (p > 0.05). Among those with and without acute exacerbations, 87.5 and 50% had poor sleep quality, respectively (p = 0.0001), with OR of 1.75 (95% CI 1.25-2.43). The age, gender, EDSS, and disease duration did not associate with sleep quality in either groups (p > 0.05). Conclusions: This study showed that sleep disturbance might be a trigger for an acute MS exacerbation. Increasing the awareness of specialists and routine screening of sleep disorders in MS patients are warranted, as treatment of these disorders might decrease the likelihood of acute relapses.

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“…Recent data from our laboratory indicated that NZB/ NZWF1 mice, an animal model of severe SLE, submitted to SD exhibit an earlier onset of the disease reflected by increased number of antinuclear autoantibody, nonetheless the mechanisms underlying these effects remain unclear [12] .…”

mentioning

confidence: 99%

Effect of Sleep Deprivation on the Corticosterone Secretion in an Experimental Model of Autoimmune Disease

Palma

Suchecki

Catallani

et al. 2007

Neuroimmunomodulation

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Objective: Sleep disturbances have been observed in a number of chronic inflammatory conditions, such as systemic lupus erythematosus. Previous results from our laboratory showed that when NZB/NZWF1 mice, an experimental model of lupus, are submitted to sleep deprivation (SD), they exhibit an earlier onset of the disease. Sleep disturbances have far-reaching effects on the endocrine and immune system, changes that may be linked to disease manifestation. Immunoendocrine communication via the hypothalamic-pituitary-adrenal axis has been proposed as an important modulatory factor for the development of autoimmune disease. We hypothesized here that corticosterone (CORT) could be involved in earlier onset of the disease in sleep-deprived NZB/NZWF1 mice. Methods: The profile of CORT secretion was measured immediately after the end of SD (platform method) and during the development of the disease. Also, we analyzed the effects of SD on CORT secretion of Swiss albino mice, which do not present immune alterations. Results: The results showed that NZB/NZWF1 mice exhibited a CORT response to SD similar to Swiss albino mice. However, CORT levels remained elevated throughout the whole period of evaluation. There was an increase in circulating levels of CORT in the NZB/NZWF1 mice as the disease progressed, but this effect was more evident in the sleep-deprived mice. Conclusion: According to these results, we suggest that elevated CORT levels are involved in the earlier onset of the disease.

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Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus

Abstract: . Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus.

Cited by 60 publications

References 54 publications

Effects on prolactin secretion and binding to dopaminergic receptors in sleep-deprived lupus-prone mice

Effects on prolactin secretion and binding to dopaminergic receptors in sleep-deprived lupus-prone mice

Sleep Disorder as a Triggering Factor for Relapse in Multiple Sclerosis

Effect of Sleep Deprivation on the Corticosterone Secretion in an Experimental Model of Autoimmune Disease

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