The Effect of Low-Dose Acetylsalicylic Acid on Cellular Immune Responses to Experimental Sleep Restriction in Healthy Humans.

INTRODUCTION

Sleep deficiency is known to increase the risk for multiple disease conditions involving immunopathology, in which inflammation is thought to be a mechanism for disease development. Thus, one potential way to mitigate negative health consequences of deficient sleep is to target inflammation. We investigated whether low-dose acetylsalicylic acid (ASA, aspirin) administration prior to and during exposure to an experimental sleep restriction challenge affects cellular immune responses to sleep restriction.

METHODS

We studied 46 healthy humans (19F/27M, age range 19-63 years) in a randomized trial with 3 protocols each consisting of a 14-day at-home phase followed by an 11-day (10-night) in-laboratory stay (sleep restriction/ASA, sleep restriction/placebo, control sleep/placebo) with daily ASA (81 mg/day) or placebo intake across the entire study period (at-home and in-laboratory). During in-laboratory stays, sleep opportunity under both sleep restriction conditions was 8 h during 2 pre-challenge nights, 4 h during 5 nights of restricted sleep, and 8 h during 3 nights of recovery sleep. Under the control sleep condition, participants had a sleep opportunity of 8 h/night throughout the protocol. Blood samples were analyzed prior to and following 5 nights of sleep restriction/control sleep, and after 2 nights of recovery sleep. Data were analyzed using generalized linear mixed models.

RESULTS

Experimental sleep restriction increased WBC, lymphocyte, monocyte, eosinophil, basophil, CD4 T-cell counts, and the CD4/CD8 T-cell ratio compared to control sleep under placebo (p < 0.01). Low-dose ASA had no effect at pre-challenge for most cell types. However, low-dose ASA attenuated the eosinophil and basophil responses to sleep restriction and reduced elevation of the CD4/CD8 T-cell ratio (p < 0.01). Monocyte counts stayed elevated after 2 nights of recovery sleep in the sleep restriction/ASA condition compared to control sleep, whereas monocyte counts recovered under placebo intake (p < 0.01).

CONCLUSION

The present study shows that low-dose ASA can counteract certain cellular immune responses to sleep restriction, in particular elevations in eosinophil and basophil counts as well as the CD4/CD8 T-cell ratio, while not affecting most immune cell counts prior to the sleep restriction challenge.