Sleep-deprivation reduces NK cell number and function mediated by beta-adrenergic signalling

Author(s)

De Lorenzo, Beatriz H. P. ^{[1, 2]} ; Marchioro, Lais de Oliveira ^[1] ; Greco, Carollina Ribeiro ^[1] ; Suchecki, Deborah ^[1]

Affiliation

^[1] Univ Fed Sao Paulo, Dept Psychobiol, BR-04024002 Sao Paulo, SP - Brazil

^[2] Ctr Univ Sao Camilo, BR-04263200 Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: PSYCHONEUROENDOCRINOLOGY; v. 57, p. 134-143, JUL 2015.
• Web of Science Citations: 10

Abstract

Reduction of steep time triggers a stress response, leading to augmented levels of glucocorticoids and adrenaline. These hormones regulate components of the innate immune system such as natural killer (NK) and NKT cells. In the present study, we sought to investigate whether and how stress hormones could alter the population and function of NK and NKT cells of mice submitted to different lengths of paradoxical sleep deprivation (PSD, from 24 to 72 h). Results showed that 72h of PSD decreased not only NK and NKT cell counts, but also their cytotoxic activity against B16F10 melanoma cells in vitro. Propranolol treatment during PSD reversed these effects, indicating a major inhibitory rote of beta-adrenergic receptors (beta-AR) on NK cells function. Moreover, both corticosterone plasma levels and expression of beta 2-adrenergic receptors (beta(2)-AR) in NK cells increased by 48 h of PSD. In vitro incubation of NK cells with dexamethasone augmented the level of beta(2)-AR in the cell surface, suggesting that glucocorticoids could induce beta(2)-AR expression. In summary, we propose that reduction of NK and NKT cell number and cytotoxic activity appears to be mediated by glucocorticoids-induced increased expression of beta(2)-AR in these cells. (C) 2015 Elsevier Ltd. All rights reserved. (AU)

• FAPESP's process: 08/06036-9 - Effect of maternal separation and maternal deprivation on the growth and metastatization of murine melanoma B16F10 and on the immune response regulation: analysis of hipotalamic-pituitary-adrenal axis activation
• Grantee: Beatriz Helena Pizarro de Lorenzo
• Support Opportunities: Scholarships in Brazil - Post-Doctoral