Objective
This study examines the reciprocal associations between sleep macrostructure and levels of cellular inflammation in rheumatoid arthritis (RA) patients and controls.
Methods
RA patients (n=24) and matched controls (n=48) underwent all-night polysomnography (PSG), along with assessment of spontaneous- and Toll-like receptor (TLR)-4 stimulated monocytic production of tumor necrosis factor-α (TNF) and interleukin (IL)-6 at 23:00 and 8:00.
Results
As compared to controls, RA patients showed lower levels of sleep efficiency (mean ± SD, 88.1 ±6.1 vs. 83.8 ± 7.0), a higher percentage Stage 3 sleep (9.3 ± 6.4 vs. 13.1 ± 6.9), and higher levels of percentage of monocytes either spontaneously expressing TNF at 23:00 (log transformed, 1.07 ± 0.28 vs. 1.22 ± 0.17), and higher TLR4 stimulated production of IL6 at 8:00 (log transformed, 3.45 ± 0.80 vs. 3.83 ± 0.39). Higher levels of stimulated production of TNF at 23:00 were associated with higher sleep efficiency (.74). In turn, sleep efficiency had a countervailing relationship on TNF production at 8:00 (. 64). Higher levels of spontaneous and stimulated production of IL6 at 23:00 were associated with more Stage 3 (.39), 4 (.43), and slow wave sleep (.49), with evidence that Stage 4 had a countervailing relationship on IL6 production at 8:00 (.60).
Conclusion
RA patients show evidence of sleep fragmentation, greater sleep depth, and higher levels of cellular inflammation. Sleep maintenance and sleep depth show countervailing relationships with evening- and morning levels of monocytic production of TNF and IL-6, respectively, which support the hypothesis of a feedback loop between sleep maintenance, slow wave sleep and cellular inflammation that is cytokine specific.