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

Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus. Am J Physiol Regul Integr Comp Physiol 291: R1527-R1532, 2006. First published June 29, 2006; doi: 10.1152/ajpregu.00186.2006.-Sleep is hypothesized to play a restorative r...

Descripción completa

Detalles Bibliográficos
Autores: Palma, Beatriz Duarte, Gabriel, Alexandre, Colugnati, Fernando A. B., Tufik, Sergio [UNIFESP]
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2006
País:Brasil
Institución:Universidade Federal de São Paulo (UNIFESP)
Repositorio:Repositório Institucional da UNIFESP
Idioma:inglés
OAI Identifier:oai:repositorio.unifesp.br:11600/29221
Acceso en línea:http://dx.doi.org/10.1152/ajpregu.00186.2006
http://repositorio.unifesp.br/handle/11600/29221
Access Level:acceso abierto
Palabra clave:sleep
New Zealand Black/New Zealand White F-1 mice
antinuclear antibody
Descripción
Sumario:Effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus. Am J Physiol Regul Integr Comp Physiol 291: R1527-R1532, 2006. First published June 29, 2006; doi: 10.1152/ajpregu.00186.2006.-Sleep is hypothesized to play a restorative role on immune system. in addition, disturbed sleep is thought to impair host defense mechanisms. Chronic sleep deprivation is a common occurrence in modern society and has been observed in a number of chronic inflammatory conditions, such as systemic lupus erythematosus (SLE). New Zealand Black/New Zealand White (NZB/NZW) F-1 mice develop an autoimmune disease that strongly resembles SLE in humans, exhibiting high titers of antinuclear antibodies associated with the development of rapidly progressive and lethal glomerulonephritis. On the basis of this evidence, the present study examined the onset and progress of lupus in as-yet healthy female mice submitted to sleep deprivation. Sleep deprivation was accomplished by two 96-h periods in the multiple-platform method when mice were 10 wk old, and they were observed until 28 wk of age. Blood samples were collected from the orbital plexus fortnightly to evaluate serum antinuclear antibodies and anti-double-stranded DNA. Proteinuria and longevity as well as body weight were also assessed. the results indicated that mice submitted to sleep deprivation exhibited an earlier onset of the disease, as reflected by the increased number of antinuclear antibodies. However, no statistical difference was found in the other parameters analyzed. According to these results, sleep deprivation could be considered as a risk factor for the onset but not for the evolution of the disease.