Gene expression and ELISA data

<p><span>O</span><span>bstructive sleep apnea is increasing worldwide, leading to disordered sleep patterns and inflammatory responses in brain and peripheral tissues that predispose individuals to chronic disease. Pro-inflammatory cytokines activate the inflammatory response and their increased expression is observed among mice exposed to experimental sleep fragmentation. Additionally, glucocorticoids are often secreted from the adrenal cortices during sleep loss and are well known to regulate inflammation. However, the temporal dynamics of inflammatory responses and hypothalamic-pituitary-adrenal (HPA) axis activation in relation to acute sleep fragmentation (ASF; 1-24h) are unknown. Male C57BL/6J mice were exposed to ASF or control conditions (no ASF) over specified time intervals (1, 2, 6, and 24 h) to elucidate the timing of onset of glucocorticoid release and pro-inflammatory responses. Cytokine gene expression (IL-1</span><span>b</span><span>, TNF-</span><span>a</span><span>) in brain and peripheral tissues and serum glucocorticoid and interleukin-6 (IL-6) concentration were measured to determine the temporal relationships of neuroendocrine-immune responses to acute SF. The HPA axis was rapidly activated, leading to elevated serum corticosterone from 1-24 h of ASF compared with controls</span><span>. This activation was followed by elevated serum IL-6 concentration from 2–24 h of ASF. The tissue to first exhibit increased pro-inflammatory gene expression from ASF was the heart (1 h of ASF). In contrast, pro-inflammatory gene expression was suppressed in the hypothalamus after 1 h of ASF, but elevated after 6 h. Because the HPA axis was elevated throughout ASF, this suggests that brain, but not peripheral, pro-inflammatory responses were rapidly inhibited by glucocorticoid immunosuppression. Instead, activation of the sympathetic nervous system (SNS) may potentiate inflammation in the short-term for peripheral tissues, but further empirical studies are needed. Understanding the mechanisms underlying the onset of inflammatory responses to sleep fragmentation could provide new therapeutic options to individuals coping with sleep disorders.</span></p>