Inflammatory bowel disease is a group of chronic medical conditions comprising Crohn's disease and ulcerative colitis that involves increased frequency of mental disorders. The most common psychiatric disorders in inflammatory bowel disease are depression and anxiety, however, some epidemiologic and biological evidence suggest that other disorders like bipolar disorder occur more often. Biological mechanisms concerning both inflammatory bowel disease and depression or anxiety explain susceptibility to developing mental disorders in inflammatory bowel disease. Interactions of brain gut-axis, immunological disturbances, oxidative stress and vagus nerve dysfunction play a role in pathophysiology of inflammatory bowel disease and mental disorders as well. Significance of these factors was covered in this paper. Psychiatric comorbidity in IBD may affect course of intestinal disease. It can increase requency and severity of relapses and hinder the treatment so knowledge about relationship between IBD and mental health appears to be vital for proper management of patients with inflammatory bowel disease.
Depression is associated with an altered immune response, which could be normalized by antidepressant drugs. However, little is known about the influence of antidepressants on the peripheral immune response and function of macrophages in individuals not suffering from depression. Our studies were aimed at determining the influence of antidepressant drugs on the humoral and cellular immune response in mice. Mice were treated intraperitoneally with imipramine, fluoxetine, venlafaxine, or moclobemide and contact immunized with trinitrophenyl hapten followed by elicitation and measurement of contact sensitivity by ear swelling response. Peritoneal macrophages from drug-treated mice were either pulsed with sheep erythrocytes or conjugated with trinitrophenyl and transferred into naive recipients to induce humoral or contact sensitivity response, respectively. Secretion of reactive oxygen intermediates, nitric oxide, and cytokines by macrophages from drug-treated mice was assessed, respectively, in chemiluminometry, Griess-based colorimetry and enzyme-linked immunosorbent assay, and the expression of macrophage surface markers was analyzed cytometrically. Treatment of mice with fluoxetine, venlafaxine, and moclobemide results in suppression of humoral and cell-mediated immunity with a reduction of the release of macrophage proinflammatory mediators and the expression of antigen-presentation markers. In contrast, treatment with imipramine enhanced the humoral immune response and macrophage secretory activity but slightly suppressed active contact sensitivity. Our studies demonstrated that systemically delivered antidepressant drugs modulate the peripheral humoral and cell-mediated immune responses, mostly through their action on macrophages. Imipramine was rather proinflammatory, whereas other tested drugs expressed immunosuppressive potential. Current observations may be applied to new therapeutic strategies dedicated to various disorders associated with excessive inflammation.
Growing number of studies suggests link between circadian rhythms and inflammatory bowel diseases (IBD) manifestation. We hypothesize that: 1) IBD are associated with increased eveningness and sleep disturbances; 2) eveningness and sleep disturbances are related to more severe IBD symptoms. In total, 129 participants were enrolled to this study, divided into three groups: 34 Crohn's disease (CD) patients, 38 ulcerative colitis (UC) patients and 57 healthy controls (HC) group. They all fulfilled a questionnaire, consisting of the Composite Scale of Morningness (CSM), Seasonal Pattern Assessment Questionnaire (SPAQ), Pittsburgh Sleep Quality Index, Inflammatory Bowel Disease Questionnaire (IBDQ) and Multidimensional Fatigue Inventory (MFI). Multiple regression models controlled for age and sex revealed that in CD group higher eveningness measured with CSM was associated with higher general fatigue, physical fatigue, mental fatigue and reduced motivation measured by MFI. Lower CSM morning affect is associated with greater general fatigue, physical fatigue and more reduced activity. Greater seasonality scores are associated with increased physical fatigue and more reduced activity and motivation. Lower sleep quality measured with PSQI is associated with higher physical fatigue and more reduced activity. Correlational analysis revealed that higher seasonality and lower sleep quality are associated with increased systemic and bowel symptoms and decreased emotional and social functions measured with IBDQ. In UC group, eveningness is associated with greater general fatigue, physical fatigue and more reduced activity. Higher CSM morning affect is associated with decreased general fatigue, physical fatigue and less reduced activity. Higher CSM circadian preference scores are associated with decreased general and physical fatigue, and less reduced activity. Increased seasonality is associated with more physical fatigue. Lower sleep quality is associated with greater general and physical fatigue. To our best knowledge this is the first study evaluating associations between chronotype and sleep disturbances with IBD symptoms. We have found that chronotype preferences, whose role in IBD has been until now overlooked, may be one of the important factors contributing to fatigue in this clinical group.
Objective: Vitamin D plays an important role in mineral turnover and bone remodeling and there are increasing data about its immunomodulatory potential in different rheumatologic disorders. Deficiency of vitamin D is frequent in patients with spondyloarthritis (SpA) and some data suggest its association with increased disease activity and structural damage. However, its exact role in the pathogenesis of SpA and its association with disease activity are still a matter of debate. Material and methods: A cross-sectional study of patients diagnosed with axial spondyloarthritis (axSpA) and peripheral spondyloarthritis (perSpA) according to Assessment of Spondyloarthritis International Society classification criteria was performed. The correlation between concentration of 25-hydroxyvitamin D-25(OH)D-and disease activity scores (Bath Ankylosing Spondylitis Disease Activity Index-BASDAI, Ankylosing Spondylitis Disease Activity Score-ASDAS), inflammatory markers (C-reactive protein-CRP, erythrocyte sedimentation rate-ESR) and clinical symptoms (arthritis, enthesitis, dactylitis) was performed. Results: We included 40 patients with axSpA and 23 patients with perSpA. The mean concentration of 25(OH)D was 24.9 ng/ml (SD 12.49). Forty-seven (74.6%) patients had 25(OH)D below the recommended threshold (< 30 ng/ml). We found no statistically significant negative correlation between the level of 25(OH)D and disease activity of axSpA and perSpA in terms of clinical symptoms (arthritis, enthesitis, dactylitis), inflammatory markers (ESR, CRP) and disease activity scores (BASDAI, ASDAS). These results did not change after adjustment for supplementation of vitamin D and seasonal variation. Conclusions: Our data show no correlation between the concentration of 25(OH)D in the serum and disease activity in two subgroups of SpA. However, this does not exclude the potential role of vitamin D in pathogenesis of SpA. Further studies are required to evaluate the optimal range of 25(OH)D serum concentration in axSpA and perSpA patients with its possible immunomodulatory potential and influence on disease activity.
SummaryThe microbiome co-evolved with its human host over a long time and became essential for many processes. Bacteria play a role in maintaining human health as they digest food, produce vitamins and participate in the regulation of metabolism. By influencing the cytokine balance along with the composition and activity of leukocytes, they constantly interact with the immune system, affecting innate and adaptive immune homeostasis. A growing number of studies indicate that the microbiome in the human intestine may have an impact on the functions of the central nervous system (CNS), through identified pathways called the gut-brain axis. Recent data show that the human microbiome ecosystem interferes with the brain's development, central signaling systems and behavior. It has been proposed that disruption in the human microbiome may affect the course of psychiatric disorders. The aim of this review is to summarize the recognized pathways of the gut-brain axis that have been thoroughly studied in animal models and to evaluate the role of the dialogue between the microbiota and the central nervous system in schizophrenia, bipolar disorder and depression. microbiome/gut-brain axis/vagus nerve/neurotransmission/hypothalamic-pituitary-adrenal (HPA) axis
The rapid development of COVID-19 vaccines became essential for addressing the global pandemic. Reactive arthritis after vaccination has been a rare phenomenon. Here, we present a case series of three patients with joint inflammation possibly attributed to COVID-19 immunization (mRNA and live adenovirus vectored vaccine). Symptoms were alleviated using non-steroid anti-inflammatory drugs and glucocorticoids. After follow-up, the patients have not been diagnosed with any other rheumatic disease. Reactive arthritis after the COVID-19 vaccine is an unusual adverse effect and poses a negligible risk in comparison to the benefits of immunization, but it should be considered in differential diagnostics by a practicing rheumatologist who cares for patients with new-onset arthritis without apparent cause at the time of pandemic.
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