![]() ![]() The level of immune cells during a 24-h day depends both on circadian and homeostatic sleep regulations through hormone and neural innervations ( 14). cortisol and pro-inflammatory cytokines) ( 11– 13). Increasing laboratory-based scientific evidence indicates that the repetition of a pattern of sleep restriction and recovery per se disrupts several physiological homeostatic and circadian mechanisms including insulin resistance, pain-related symptoms or stress and immune dysregulations (e.g. In addition, in order to compensate for the extended “daily” wakefulness durations, shift workers frequently ‘catch up’ on sleep on free days. The role of the desynchronization of the circadian clock from night shift work begins to be well established for the pathogenesis of breast and other cancers, as well as for metabolic, cardiovascular and infectious diseases ( 5– 10). Indeed, shift and night workers are chronically poor sleepers, with shortened sleep durations and have to cope both with sleep debt and with circadian desynchronization ( 2– 4). Thus, many shift workers sleep at the “wrong” physiological time, because of the odd timing of imposed sleep episodes related to the work schedules. Changes in work timing schedules frequently disrupt the tight links between the circadian rhythms that drive and regulate sleep, and sleep processes. Shift work including night work involves 15-20% of the total working population in the world (WHO, 2020) ( 1). Specifically, these altered pattern expressions of immune cells may increase vulnerability to infections and reduce vaccination efficiency in night workers. In contrast, among night shifters, multivariate analyses indicated a combined effect of total sleep time (TST24w), sleep debt and social jet-lag for total lymphocytes and T-helper cells but only a social jet-lag effect for interleukin-6 and a single total sleep time effect for neutrophil and B-Cells.Ĭonclusions: Altogether, our results point to intricate response patterns of immune rhythms to circadian misalignment and sleep debt in night shifters. Multivariate analyses ruled out significant impact of TST24w, sleep debt, and social jet-lag on immune biomarkers concentrations among day shifters. By contrast, in night shifters, blood concentrations of total lymphocytes, T-helper cells, cytotoxic T-cells, memory B-cells and interleukin-6 were lower at 21:00, increased during the night, and reached higher values at 7:00. Variations of immune biomarkers concentrations were consistent with the expected diurnal variations among day shifters (i.e., low level in the morning, increase during the day, peak value in the evening). Results: Compared with day shifters, night shifters had shorter sleep duration (TST24w=5.4 ± 1.4h), greater sleep debt (3.2 ± 1.4 h) and social jet-lag (6.7 ± 2.4 h). Circulating blood counts in immune cells, interleukin-6 and C-reactive protein concentrations as well as total sleep time per 24 hours during work days (TST24w) and free days (TST24f), sleep debt (TST24f - TST24w) and social jet-lag (a behavioral proxy of circadian misalignment) were assessed. Blood samples were collected at the beginning and end of the last shift during the week, and participants were categorized into three groups based on work shift: morning shift (39 day shifters sampled at 7:00 and 14:00), afternoon shift (57 day shifters sampled at 14:00 and 21:00), and night shift (95 night shifters sampled at 21:00 and 7:00). ![]() Methods: Hospital nurses working either as permanent night shifters (n=95) or as day shifters rotating between morning and afternoon shifts (n=96) kept a daily diary on their sleep and work schedules over a full working week. Objectives: We aimed to examine the effects of circadian and sleep rhythm disruptions on immune biomarkers among hospital healthcare professionals working night shifts and rotating day shifts. ![]()
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