Gene expression and ELISA data

Obstructive 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-1b, TNF-a) 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. 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.