A Quadruple Relationship: Sleep, Immune System, Inflammation and Psychiatric Disorders

Sleep is an important part of life and its quality is indispensable to a number of brain functions, including communication of neurons and therefore maintenance of brain health. Several studies have systematically demonstrated adverse effects when sleep behavior is compromised. Inadequate amount of sleep may cause: emotional and cognitive impairment. Sleep is regulated by the circadian system that times daily sleep which is driven by an internal timing system. Clock genes control rhythms in physiology and behavior which are associated with sleep and wakefulness and transcriptional level of them leads the gene networks that are released with a 24-hour cycle (1). It has been accepted that disruption of circadian rhythms is associated with sleep disorders, and some chronic diseases including infectious diseases, autoimmune diseases, metabolic syndrome, neurodegenerative diseases. It is also highlighted that coordination between circadian clock of immune response through innate and adaptive immune cells and a regulatory layer relative to circadian clock. Inflammation based disorders such as infections can disrupt the circadian clock and reduce the amplitude of circadian rhythms significantly. Results obtained from autoimmune disease models neuroinflammation and demyelination may be due to an increase in pathogenic T lymphocytes showing the involvement of inflammation (2). Sleep is known to play an important role in immune function. However, the effects of sleep quality during hospitalization for COVID-19 remain unclear was investigated in a retrospective, single-center cohort study. It was conducted to investigate the effects of sleep quality on recovery from lymphopenia and clinical outcomes in hospitalized patients with laboratory-confirmed COVID-19. It has been found that poor sleep quality during hospitalization in COVID-19 patients with lymphopenia is associated with a slow recovery from lymphopenia and an increased need for ICU care (3). It has been accepted that sleep problems are the most prominent symptom among with psychiatric disorders including major depressive disorder (MDD), bipolar disorder (BD), generalized anxiety disorder, post-traumatic stress disorder (PTSD), schizophrenia etc. In approximately 90% of depressive patients have some types of sleep disorder (sleep apnea syndrome, insomnia, parasomnias, restless legs syndrome etc.). Therefore, psychiatric disorders have an impact on sleep, sleep disorders have an impact on psychiatric conditions, treating sleep disorders. MDD has been associated with the decreased REM sleep latency. Transition into REM sleep is accompanied by a rapid decrease in monoamines such as serotonin [5‐HT], norepinephrine [NE] and dopamine and an increase in cholinergic activity. It is known that bi-directional interaction of cholinergic and monoaminergic neurons regulates the onset of REM sleep and main cause of depression is significant reduction of monoaminergic neurotransmitters (mainly 5‐HT and NE) (4-6). About 80 percent of depressive patients suffer from impaired sleep which show characteristic sleep-EEG changes such as impaired sleep continuity, disinhibition of REM sleep and changes in non-REM sleep. In the hypothalamus, the suprachiasmatic nucleus (SCN) which increases production of the hormone melatonin in order to trigger sleep is important for matching the body’s circadian rhythm to the external cycle of light and darkness through pineal gland. In communication with the brain stem, especially the pons and medulla, thalamus, cerebral cortex, basal forebrain and midbrain regulates sleep and wakefulness whereas the amygdala is involved in sleep more related with the mood (4). Recent accumulating data support a key role of gut microbiota, food intake and pathogen-associated molecular patterns (PAMPs) in triggering production of inflammatory mediators causing sleep changes. Environment, including stress, physical activity, and food intake can increa