Study Objectives: Obstructive sleep apnea (OSA) is a chronic condition that is characterized by recurrent pauses in breathing during sleep causing intermittent hypoxia. The main factor responsible for oxygen metabolism homeostasis is hypoxia-inducible factor 1 (HIF-1), comprised of 2 subunits: α (oxygen sensitive) and β. The aim of the study was to investigate the HIF-1α serum protein level and mRNA HIF-1α expression in patients with OSA and a healthy control group and determine their evening-morning variation and association with polysomnography parameters. Methods: Eighty-four individuals were enrolled in the study. All patients underwent polysomnography examination and based on the results were divided into 2 groups: OSA group (n = 60) and control group (n = 24). Peripheral blood was collected in the evening before and in the morning after the polysomnography. HIF-1α expression was evaluated on protein in blood serum and mRNA level in peripheral blood leukocytes. Results: HIF-1α serum protein concentration was higher in patients with OSA compared with control patients in both the evening (1,490.1 vs. 727.0 pg/mL; P <.001) and the morning (1,368.9 vs. 702.1 pg/mL; P <.001) samples. There was no difference between evening and morning HIF-1α serum protein level in either group. No differences were observed in HIF-1α mRNA expression between the OSA and control group. Additionally, evening and morning HIF-1α serum protein level correlated with number of desaturations during sleep (r = .384, P < .001 and r = .433, P < .001, respectively). Conclusions: Observed differences in HIF-1α serum protein level between the OSA and the control groups without difference between evening and morning measurements suggest chronic increase in this protein concentration by intermittent nocturnal hypoxia in OSA.

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia and associated with the disruption of circadian rhythm. The study aimed to assess the relationship between hypoxia-inducible factor (HIF) subunits, circadian clock proteins, and polysomnography (PSG) variables, in healthy individuals and severe OSA patients. The study included 20 individuals, who underwent PSG and were divided into severe OSA group (n = 10; AHI ≥ 30) and healthy control (n = 10; AHI < 5) based on apnea-hypopnea index (AHI). All participants had their peripheral blood collected in the evening before and the morning after the PSG. HIF-1α, HIF-1β, BMAL1, CLOCK, CRY1, and PER1 protein concertation measurements were performed using ELISA. In a multivariate general linear model with the concentration of all circadian clock proteins as dependent variables, evening HIF-1α protein level was the only significant covariant (p = 0.025). Corrected models were significant for morning and evening PER1 (p = 0.008 and p = 0.006, respectively), evening (p = 0.043), and evening BMAL protein level (p = 0.046). In corrected models, evening HIF-1α protein level had an influence only on the evening PER1 protein level. Results suggest that OSA patients are at risk for developing circadian clock disruption. This process might be mediated by subunit α of HIF-1, as its increased protein level is associated with overexpression of circadian clock proteins.

The causes of disordered sleep, frequently reported by patients with inflammatory bowel diseases (IBD), are poorly understood. The study aimed to evaluate sleep quality in IBD patients and to identify factors affecting their sleep. IBD patients (n = 133) and healthy controls (HC; n = 57) were included in the study and completed sleep questionnaires (Pittsburgh Sleep Quality Index (PSQI), Athens insomnia scale (AIS), and Epworth sleepiness scale (ESS)), Beck Depression Inventory (BDI), and pain scales (Visual Analogue Scale and Laitinen Pain Scale). IBD patients attained higher scores in all sleep questionnaires compared to HC: PSQI, AIS, and ESS (all p < 0.001). They also had prolonged sleep latency (p < 0.001) with reduced sleep efficiency (p < 0.001). Patients in exacerbation of IBD had higher scores in PSQI (p = 0.008), ESS (p = 0.009), but not in AIS, compared to those in remission. Participants with comorbid chronic diseases had higher scores in PSQI and AIS, but not in ESS, compared to others. Multiple regression revealed that the sleep questionnaire results were significantly affected by mood level (BDI), but not by the aforementioned pain scales. Sleep impairment in IBD patients is a common problem that deserves attention in everyday clinical practice and mood level seems to be the main factor affecting the quality of sleep in IBD patients.

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Obstructive sleep apnea (OSA) is a recognized independent risk factor for metabolic disorders, type 2 diabetes mellites (DM2) in particular. Therefore, the study aimed to assess the influence of nocturnal oxygen saturation parameters on the onset of DM2 among OSA patients. The study consisted of 549 participants, who underwent polysomnography examination. Based on apnea hypopnea index (AHI), 465 patients were diagnosed with OSA. One hundred and seven individuals had comorbid DM2. Cox regression models were used to assess the effect of oxygen saturation parameters on the onset of DM2. Classification and regression trees (CART) analysis was used to assess the onset of the DM2 in the study group in context of oxygen saturation variables. One-way Cox regression showed higher risk of earlier DM2 for increased values of BMI, AHI, decreased basal O2 and O2 nadir value, while lowered mean O2 desaturation has not shown statistical significance. In the CART analysis, the following cut-off points 92.2%, 81.7%, 87.1% were determined for basal O2, O2 nadir and mean O2 desaturation, respectively, with the first two parameters being statistically significant. Therefore, basal O2 is independent from AHI, BMI and age is a risk factor of DM2 among OSA patients.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin regulating synaptic plasticity, neuronal excitability, and nociception. It seems to be one of the key molecules in interactions between the central nervous system and immune-related diseases, i.e., diseases with an inflammatory background of unknown etiology, such as inflammatory bowel diseases or rheumatoid arthritis. Studies show that BDNF levels might change in the tissues and serum of patients during the course of these conditions, e.g., affecting cell survival and modulating pain severity and signaling pathways involving different neurotransmitters. Immune-related conditions often feature psychiatric comorbidities, such as sleep disorders (e.g., insomnia) and symptoms of depression/anxiety; BDNF may be related as well to them as it seems to exert an influence on sleep structure; studies also show that patients with psychiatric disorders have decreased BDNF levels, which increase after treatment. BDNF also has a vital role in nociception, particularly in chronic pain, hyperalgesia, and allodynia, participating in the formation of central hypersensitization. In this review, we summarize the current knowledge on BDNF’s function in immune-related diseases, sleep, and pain. We also discuss how BDNF is affected by treatment and what consequences these changes might have beyond the nervous system.

Inflammatory bowel disease (IBD) is a group of chronic gastrointestinal disorders that include Crohn's disease (CD) and ulcerative colitis (UC). CD etiology is multifactorial and many of its aspects are still not entirely clear.Brain-derived neurotrophic factor (BDNF) belongs to the family of neurotrophins and is a factor of neuronal growth, additionally affecting the peripheral nervous system: mainly sensory and motor neurons, which are also found in the intestines. 1 It is a neuromodulator that may play an important role in the interaction between the brain and intestines. 2 BDNF has been associated with the severity of

Epidemiological studies have shown that individuals with sleep problems are at a greater risk of developing immune and chronic inflammatory diseases. As sleep disorders and low sleep quality in the general population are frequent ailments, it seems important to recognize them as serious public health problems. The exact relation between immunity and sleep remains elusive; however, it might be suspected that it is shaped by others stress and alterations of the circadian rhythm (commonly caused by for example shift work). As studies show, drugs used in the therapy of chronic inflammatory diseases, such as steroids or monoclonal antibodies, also influence sleep in more complex ways than those resulting from attenuation of the disease symptoms. Interestingly, the relation between sleep and immunity appears to be bidirectional; that is, sleep may influence the course of immune diseases, such as inflammatory bowel disease. Thus, proper diagnosis and treatment of sleep disorders are vital to the patient’s immune status and, in effect, health. This review examines the epidemiology of sleep disorders and immune diseases, the associations between them, and their current treatment and novel perspectives in therapy.