@Article{ecn.2014.0356,
AUTHOR = {Mounir Chennaoui, Catherine Drogou, Fabien Sauvet, Danielle Gomez-Merino, Denis E. Scofield, Bradley C. Nindl},
TITLE = {Effect of acute sleep deprivation and recovery on Insulin-like Growth Factor-I responses and inflammatory gene expression in healthy men},
JOURNAL = {European Cytokine Network},
VOLUME = {25},
YEAR = {2014},
NUMBER = {3},
PAGES = {52--57},
URL = {http://www.techscience.com/ECN/v25n3/65558},
ISSN = {1952-4005},
ABSTRACT = {Acute sleep deprivation in humans has been found to increase inflammatory markers and signaling
pathways in the periphery through a possible Toll-like receptor 4 (TLR-4). In addition, short duration sleep has
been associated with low circulating total Insulin-like Growth Factor-I (IGF-I) concentrations. We aimed to determine
whether a total sleep deprivation (TSD) protocol with recovery altered whole-blood gene expression of the
proinflammatory cytokines TNF-α and IL-6, as well as TLR-4 expression, and to examine the relationship with
circulating concentrations of the IGF-I system. Twelve healthy men participated in a five-day TSD (two control
nights followed by one night of sleep deprivation and one night of recovery). Blood was sampled at 0800, before and
after sleep deprivation (D2 and D4), and after recovery (D5). It is shown that 25h of sleep deprivation (D4) induced
significant increases in mRNA levels of TNF-α and its soluble receptor R1 (P<0.01 respectively), as well as TLR-4
(P<0.05), while IL-6 mRNA levels remained unchanged. Circulating concentrations of free IGF-I were decreased
at D4 (P<0.001). One night of recovery was sufficient to restore basal expression levels for TNF-α, sTNF-R1, TLR-4
and circulating IGF-I. Changes in TLR-4 mRNA levels during the protocol correlated positively with those of
TNF-α and sTNF-R1 (r = 0.393 and r = 0.490 respectively), and negatively with circulating free IGF-I (r = -0.494).
In conclusion, 25h of sleep deprivation in healthy subjects is sufficient to induce transient and reversible genomic
expression of the pro-inflammatory cytokine TNF-α and its R1 receptor, and its mediator TLR-4, with a possible
link to IGF-I axis inhibition.},
DOI = {10.1684/ecn.2014.0356}
}