Der Einfluss von experimentell induzierten, insomnieartigen Symptomen auf Interleukin-6 und Lymphozytensubpopulationen
Immunologie
Kognitive, systemische und Verhaltensneurobiologie
Zusammenfassung der Projektergebnisse
Sleep disturbances as seen in insomnia disorder are associated with increases in inflammatory markers. To investigate whether these inflammatory changes are causally related to the characteristic sleep patterns of insomnia patients (including delayed sleep onset, frequent nocturnal awakenings, early morning awakening), we measured the inflammatory response to a newly developed model of experimentally induced insomnia ymptoms (EIIS) in healthy humans. Twenty-four healthy volunteers (age: 27.9 plus minus 1.2 years; 50% women) participated in a within-subjects study including two 19-day in-hospital stays. During the EIIS condition, three nights with an 8-hour sleep opportunity (23:00 - 07:00h) were followed by three cycles of three nights with sleep disruption (EIIS nights) and one night of recovery sleep. During EIIS nights, sleep onset was delayed and sleep offset advanced by one hour and sleep time was interrupted by hourly 20-min awakenings. During recovery nights as well as during the control condition, undisturbed sleep was allowed for 8 hours. Lipopolysaccharide (LPS)-stimulated and unstimulated production of interleukin (IL)-6 in monocytes, C-reactive protein (CRP) levels in plasma and the number of leukocytes and various leukocyte subsets were measured in blood collected at 11:00h on selected EIIS and recovery nights of each cycle. As expected, the model effectively increased sleep onset latency and reduced sleep efficiency. In contrast to our hypothesis, CRP levels and unstimulated IL-6 production in monocytes were reduced in the EIIS condition compared to control. No effect was observed on LPS-stimulated IL-6 production, IL-6 levels in plasma, and the absolute number of leukocytes and leukocyte subsets. The findings of reduced rather than increased inflammatory markers in the EIIS condition were surprising. This might indicate that the inflammatory system over-compensates any disturbances induced by the EIIS protocol in our healthy, young participants. This regulation might fail after chronic sleep disruption as seen in insomnia patients. Future studies should include repeated blood samplings during the night and the day to allow the characterization of the effects of sleep disruption on inflammatory markers at different times of the day and possible compensatory mechanisms.
