Chemical sympathectomy reduces peripheral inflammatory responses to acute and chronic sleep fragmentation.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Ila MishraNoah T Ashley

Abstract

Sleep loss contributes to the development of cardiovascular, metabolic, and neurological disorders by promoting a systemic proinflammatory phenotype. The neuroendocrine-immune mechanisms contributing to such pathologies are poorly understood. The sympathetic nervous system (SNS) regulates immunity and is often activated following sleep disturbances. The aims of this study were to determine 1) the effect of SNS inhibition on inflammatory responses to sleep fragmentation (SF) and 2) whether homeostasis can be restored after 1 wk of recovery sleep. We measured stress responses (norepinephrine and corticosterone), gene expression levels of pro- and anti-inflammatory cytokines in peripheral (heart, liver, and spleen) tissues, and protein levels of cytokines and chemokines in serum of female mice that were subjected to acute SF for 24 h, chronic SF for 8 wk, or 7 days of recovery after chronic SF. In each experiment, SF and control mice were chemically sympathectomized with 6-hydroxydopamine (6-OHDA) or injected with vehicle. Both acute and chronic SF elevated mRNA and protein levels of cytokines in peripheral tissues. Changes in inflammatory responses mirrored stress-axes activation, with increased corticosterone and norepinephrine ...Continue Reading

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Citations

Oct 17, 2020·American Journal of Physiology. Heart and Circulatory Physiology·Joshua M CherubiniMaureen J MacDonald
Sep 18, 2021·Stem Cell Research & Therapy·Shiguo YuanXiaochun Bai

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