Sleep And Immunity Relationship With Inflammatory Response Part 2

Similar changes were seen even in a child population, regardless of sex. However, the influence of reduced sleep duration on telomere length might be indirect, as inflammatory cytokines may themselves have this effect. 

Proinflammatory cytokines are protein molecules that activate inflammatory responses and play an important role in the human immune system. Although proinflammatory cytokines can initiate inflammatory responses, inflammatory responses are also part of the normal response of the immune system.

When the body is infected or injured, the immune system releases proinflammatory cytokines to activate inflammatory responses to protect the body from further damage and destruction. In addition, proinflammatory cytokines can also help regulate many other immune responses, including enhancing the vitality of immune cells and increasing their ability to fight pathogens.

However, if proinflammatory cytokines are produced too much or last too long, it will lead to excessive inflammatory responses, which will hurt human health. For example, excessive inflammatory responses may cause arthritis, lupus erythematosus, and other autoimmune diseases, and may even induce dangerous diseases such as cancer.

Therefore, it is very important to keep the immune system in balance. We should pay attention to good habits such as diet, regular work rest, and keep a cheerful mood to enhance our resistance and prevent excessive inflammatory responses from negatively affecting our health. In addition, for some diseases that require controlled immune responses, such as rheumatoid arthritis and lupus erythematosus, specific drug treatments can be used to control the production of proinflammatory cytokines. It can be seen that we need to improve memory, and Cistanche can significantly improve memory because it has antioxidant, anti-inflammatory, and anti-aging effects, which can help reduce oxidation and inflammatory reactions in the brain, thereby protecting the health of the nervous system. In addition, Cistanche can also promote the growth and repair of nerve cells, thereby enhancing the connectivity and function of neural networks. These effects can help improve memory, learning ability, and thinking speed, and can also prevent the occurrence of cognitive dysfunction and neurodegenerative diseases.

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 There is a relationship between measures of humoral and cellular immunity on the one hand and sleep duration on the other in the general population. 

Reduction in the usual sleep duration is accompanied by increases in the contents of proinflammatory cytokines and CRP, which in turn increases the risk of developing cardiovascular diseases and mortality. Sufficient sleep duration can determine susceptibility to infectious diseases. 

Studies reported by Patel et al. [14] showed that short (<5 h) nocturnal sleep was associated with an elevated (1.7-fold) risk of pneumonia in the next two years or the next few months. 

Another experiment involving healthy volunteers assessed the probability of contracting acute respiratory viral diseases (ARVD), depending on sleep duration. 

Young people sleeping <7 h (assessed subjectively) fell ill 2.9 times more frequently than those sleeping ≥8 h [15]. This experiment was subsequently repeated using actigraphy as a method for objective assessment of sleep duration. 

This yielded less dramatic results – even though subjects sleeping <5 h fell ill 4.2 times more frequently than those sleeping >7 h, sleep duration in the rangeof  6–7 h was not accompanied by any significant increase in the risk of illness [16]. 

A relationship between the incidence of infectious diseases (ARVD, influenza, gastritis) and sleep duration was also seen in adolescents. A model for studies of the effects of sleep on measures of adaptive immunity may be provided by experiments with vaccination of healthy volunteers with different sleep durations. 

The first study of this type addressed the effects of sleep deprivation on the formation of specific antibodies to influenza virus H1N1. Spiegel et al. [17] found that patients with normal (7–8 h) sleep plots had antibody titers 2.5 times higher than those able to sleep only 4 h for six nights. 

Further studies showed that even one night of sleep deprivation led to decreases in the titers of antibodies to hepatitis A and B and swine flu u respectively [1]. 

The positive influence of sleep on the formation of acquired immunity is linked with the effects of increases in the proinflammatory cytokine and/or effector cell population discussed above. In the long term and larger contingents of patients, increases in sleep duration also constitute a winning strategy in increasing the efficacy of vaccination. 

Thus, a study reported by Prathner et al. [18] in a group of patients undergoing three hepatitis B immunizations found a relationship between vaccination efficacy and the usual duration of sleep. 

The proportion of people attaining adequate protection as a result of vaccination (defined as a level of anti-HBs IgG ≥ 10 mIU/ml) was 3.5 times higher in the group of people sleeping >7 h than in those sleeping <6 h. Researchers have explained better immunization associated with sleep primarily in terms of the anabolic effects of prolactin and somatotropic hormones. 

Furthermore, an important role in supporting better responses is played by the "painful amatory" tuning of the cytokine system during sleep. Besedovsky et al. [1] took the view that the existence of large numbers of antigen-presenting cells and T-cells in secondary lymphoid organs during sleep will provide a better exchange of information on the incoming antigen. 

This involves a process analogous to memory consolidation in the brain – which operates better in sleep because the right conditions for it are created (detachment from external stimuli and a special mode of neuronal electrical activity in the form of slow-wave oscillations). 

In this case, the conditions involve a high probability of close contact with immunocompetent cells in secondary lymphoid organs, a proinflammatory cytokine trend, and a favorable (anabolic) hormonal background. 

The positive effect of this particular hormonal-neuronal "tuning" of the body during sleep was supported by data reported by Besedovsky et al. [19] from studies producing an artificial increase in slow-wave activity in the slow-wave sleep phase, in which a decrease in the circulating cortisol concentration and a reduction in the number of lymphocytes (interpreted by the authors as a result of their migration to secondary lymphoid organs) were seen. 

 Other approaches to the use of sleep as an immunomodulator included an attempt to evaluate the effects of an increased duration of nocturnal sleep in humans on measures of cellular and humoral immunity, and also studies of the effects of short daytime naps on these measures. 

In studies reported by Chennaoui et al. [20], sleep duration in healthy young people was increased by 1.5 h for six nights, confirmed by polysomnography data. However, there were no significant changes in the numbers of peripheral blood lymphocytes, monocytes, and neutrophils during daytime sleep. 

A pilot study reported by Haack et al. [21] in which sleep duration was assessed by actigraphy, where an increase in initially reduced (to 6 h per night) sleep duration led to minor reductions in the lymphocyte count, CRP, and IL-6. 

 More encouraging results were obtained by assessment of short daytime naps on measures of immunity. Population studies have shown that the occurrence of short daytime naps (self-reported) was associated with increased CRP and IL-6 levels, i.e., proinflammatory substances [1]. However, the experimental conditions did not allow evaluation of the direction of the causality. 

It is entirely likely that the existence of the health-burdening states accompanying increases in the levels of these substances promoted increases in the need for sleep, given that administration of IL-6 in experimental models in animals led to increases in the duration of slow-wave sleep [1]. 

 Daytime naps in controlled conditions were found to have positive influences on measures of immunity when initially decreased on the background of sleep deprivation. For example, studies reported by Vgontzas et al. [22] showed that 2-h postprandial sleep led to a decrease in elevated IL-6 and cortisol concentrations. 

In two further studies, daytime naps after significant (up to 2 h) contraction of nocturnal sleep duration were accompanied by decreases in IL-6 levels and neutrophil counts [1]. Sleep Disorders and Immunity. 

The occurrence of sleep disorders is accompanied not only by decreases in sleep duration but also by impairment of its quality. Studies reported by Donners et al. [23] in Dutch students used the sleep disorder questionnaire SLEEP-50 and self-assessed health status. 

Students who evaluated themselves as "frequently ill" had worse self-assessments of sleep and higher scores in questionnaire sections addressing sleep disorders such as insomnia, obstructive sleep apnea syndrome, and circadian rhythm sleep disorder. 

 Insomnia is a common sleep disorder, which in its chronic form affects at least 6% of the general population. The annual incidence of acute (short-term) forms of insomnia is 20% [24]. 

The structure of insomnia includes various impairments to the process of sleep or its perception (difficulty going to sleep after going to bed in the evening or after nocturnal waking, frequent nocturnal waking, feelings of shallow sleep, early morning waking, unsatisfactory sleep). 

 Consideration of the role of sleep in ensuring the normal operation of the body's immune system raises the question of whether patients with ininsomnia have abnormalities with innate or adaptive immunity. 

Apart from the Dutch study [23] noted above, which provided a very indirect assessment of immune system functioning, we found one study evaluating the role of insomnia in forming specific immunity on vaccination against influenza with a trivalent vaccine. 

Immunized students with insomnia had lower postvaccination antibody titers than those without sleep disorders [25]. The treatment of choice for insomnia is cognitive behavioral therapy (CBT-I). 

This is a multi-component method directed at teaching patients the basic concepts of the mechanisms of their sleep and the causes of its impairment and then conducting behavioral experiments based on the resulting knowledge. 

Ultimately, this avoids dysfunctional beliefs and improves sleep quality. Standard CBT-I programs consist of 6–8 weekly sessions with a qualified specialist. Studies reported by Irwin et al. [26] included CBT-I and measurement of changes in IL-6, TNF-α, and CRP levels. 

Correction of sleep impairments using this method was accompanied by decreases in all inflammation markers over a follow-up period of two months, the only improvement persisting to 16 months being CRP. 

Transcriptome studies showed decreases in the expression of the genes for these proinflammatory humoral substances during treatment, while the expression of genes involved in producing interferons and antibodies increased. 

In another study, CBT-I in women with breast tumors was accompanied by increases in lipopolysaccharide-induced IL-1 and interferon production. In two other observations, improvements in sleep during CBT-I were accompanied by decreases in circulating IL-1, CRP, and IL-18 (a pro-inflammatory cytokine of the IL-1 family) levels [1].

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