UMLS:C0011570 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic 'overshooting' with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
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PMID:Cytokine dysregulation, inflammation and well-being. 1616 5

Anti-inflammatory effect of desloratadine (DL), including, but not limited to depression of production of IL-4, IL-6 and IL-8, has been shown in several in vitro experiments but only a few in vivo studies refer to this findings. The purpose of our study was to evaluate the influence of DL on levels of IL-4, IL-10, IL-18 and TGF-beta in sera of patients with seasonal allergic rhinitis (SAR). Sixty-nine subjects suffering from SAR with hypersensitivity to grass pollen were included into the evaluation of clinical efficacy of DL (5mg once daily). None of them was taking any H(1) receptor antagonist during the pollen season before inclusion into the study. Samples of peripheral blood were taken before and after 4 weeks of treatment. Levels of cytokines were determined using the ELISA method. The mean level of IL-4 was 0.212+/-0.07pg/ml before and 0.221+/-0.1pg/ml after the treatment (p=0.52); IL-10 5.13+/-3.14 and 4.71+/-0.88 (p=0.69); IL-18 54.45+/-26.09 and 44.80+/-22.42 (p=0.48); TGF beta 949.17+/-401.5 and 955.7+/-391.2 (p=0.97)pg/ml before and after the treatment, respectively. Unless in vitro DL demonstrates not only anti-allergic but also anti-inflammatory activities data from this in vivo study in a group of patients suffering from SAR do not support previous pre-clinical findings.
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PMID:The effect of 4 weeks treatment with desloratadine (5mg daily) on levels of interleukin (IL)-4, IL-10, IL-18 and TGF beta in patients suffering from seasonal allergic rhinitis. 1653 Apr 40

Fibromyalgia (FMS) is a debilitating disorder characterized by chronic diffuse muscle pain, fatigue, sleep disturbance, depression and skin sensitivity. There are no genetic or biochemical markers and patients often present with other comorbid diseases, such as migraines, interstitial cystitis and irritable bowel syndrome. Diagnosis includes the presence of 11/18 trigger points, but many patients with early symptoms might not fit this definition. Pathogenesis is still unknown, but there has been evidence of increased corticotropin-releasing hormone (CRH) and substance P (SP) in the CSF of FMS patients, as well as increased SP, IL-6 and IL-8 in their serum. Increased numbers of activated mast cells were also noted in skin biopsies. The hypothesis is put forward that FMS is a neuro-immunoendocrine disorder where increased release of CRH and SP from neurons in specific muscle sites triggers local mast cells to release proinflammatory and neurosensitizing molecules. There is no curative treatment although low doses of tricyclic antidepressants and the serotonin-3 receptor antagonist tropisetron, are helpful. Recent nutraceutical formulations containing the natural anti-inflammatory and mast cell inhibitory flavonoid quercetin hold promise since they can be used together with other treatment modalities.
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PMID:Fibromyalgia--new concepts of pathogenesis and treatment. 1656 42

This study was designed to measure nitrite/nitrate and cytokine levels of serum obtained from septic shock patients and to describe potential depressant effects of human septic serum on rat cardiomyocytes. Serum was prepared from 10 non-septic patients and 10 patients with documented septic shock. Adult rat ventricular myocytes were exposed to 20 % serum in the medium. Cardiomyocyte contractility was assessed by measuring shortening fraction and shortening velocity. Serum levels of nitrite/nitrate, a marker of nitric oxide final metabolites, and cytokines (tumor necrosis factor (TNF)-alpha, interleukin (IL) 1beta, 6, 10, 8 and 12p70) were measured. Compared with serum from non-septic patients, serum of septic shock patients induced rapid reduction of the extent and velocity of shortening in isolated cardiomyocytes. Nitrite/nitrate, TNF-alpha, IL-1beta and IL-12p70 concentrations of tested serum for cardiomyocyte studies were not increased in septic serum compared with controls. In contrast, septic serum that induced a depression of in vitro contractility, had increased levels of IL-6, IL-8 and IL-10. We can conclude that the depression of in vitro contractility induced by septic serum is not directly dependent on elevated levels of nitric oxide metabolites, TNF-alpha or IL-1beta. Our results support the view that other cytokines, including IL-6, IL-8 and IL-10, are potent circulating mediators of myocardial depression in cardiomyocytes.
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PMID:Cytokine profile of human septic shock serum inducing cardiomyocyte contractile dysfunction. 1679 75

A growing literature suggests that psychosocial factors, such as chronic stress and depression, are associated with increased vulnerability to inflammatory disease; however, the mechanisms of this effect remain unclear. One possibility is that these psychosocial characteristics are associated with activation of innate inflammatory pathways. Here, we explore relationships between a range of psychosocial risk factors for inflammatory disease and a measure of inflammatory potential, lipopolysaccharide-induced production of the monocyte-derived proinflammatory cytokines/chemokines interleukin (IL)-1beta, IL-6, TNF-alpha, and IL-8 among a community sample of 183 healthy adults aged 30-54 years. After controlling for demographic factors, health behavior practices, blood pressure, and white blood cell count, hierarchical regression analyses revealed a positive relationship between production of IL-8 and symptoms of depression, trait negative affect, and perceived stress. In contrast, there was an inverse relationship between IL-8 production and perceived social support. Relationships between IL-8 and symptoms of depression and perceived stress were attributable primarily to dispositional differences in NA. The relationship between negative affect measures and IL-8 was independent of social support. Although there were significant univariate associations between higher IL-6 production and symptoms of depression and less social support, these relationships did not withstand adjustment for demographic controls. There were no significant associations between IL-1beta or TNF-alpha and any of the psychosocial parameters. Our findings suggest that individuals at greater psychosocial risk for the development of inflammatory diseases, including cardiovascular disease, also show greater stimulated production of the proinflammatory chemokine, IL-8. Further exploration of this potential psychophysiological pathway is warranted.
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PMID:Stimulated production of interleukin-8 covaries with psychosocial risk factors for inflammatory disease among middle-aged community volunteers. 1699 40

Migraine is a common disorder, characterized by recurrent episodes of headache and associated symptoms. The full pathophysiology of migraine is incompletely delineated. Current theories suggest that it is a neurovascular disorder involving cortical depression, neurogenic inflammation and vasodilation. Various neuropeptides and cytokines have been implicated in the pathophysiology of migraine including calcitonin gene-related peptide, interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-alpha. There is evidence demonstrating an association between migraine and processes associated with inflammation, atherosclerosis, immunity and insulin sensitivity. Similarly, adiponectin, an adipocytokine secreted by adipose tissue, has protective roles against the development of insulin resistance, dyslipidaemia and atherosclerosis and exhibits anti-inflammatory properties. The anti-inflammatory activities of adiponectin include inhibition of IL-6 and TNF-induced IL-8 formation, as well as induction of the anti-inflammatory cytokines IL-10 and IL-1 receptor antagonist. Adiponectin levels are also inversely correlated with C-reactive protein (CRP), TNF-alpha and IL-6 levels. Likewise, recent studies have shown a possible correlation between CRP, TNF-alpha and IL-6 and migraine attacks. In addition, insulin sensitivity is impaired in migraine and obesity is a risk factor for the transformation from episodic to chronic migraine. In this review we discuss the basic science of adiponectin and its potential connection to the pathophysiology of migraine. Future research may focus on how adiponectin levels are potentially altered during migraine attacks, and how that information can be potentially translated into migraine therapy.
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PMID:Migraine and adiponectin: is there a connection? 1744 81

The neuroendocrine system affects the immune system through the neuroendocrine humoral outflow via the pituitary, and through direct neuronal influences via the sympathetic, parasympathetic (cholinergic) and peptidergic/sensory innervation of peripheral tissues. Circulating hormones or locally released neurotransmitters and neuropeptides regulate major immune functions, such as antigen presentation, antibody production, lymphocyte activity, proliferation and traffic, and the secretion of cytokines including the selection of T helper (Th)1 or Th2 cytokine responses. During inflammation, the activation of the stress system, through induction of a Th2 shift protects the organism from systemic "overshooting" with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones, substance P, ATP and the activation of the corticotropin-releasing hormone/substance P-histamine axis may actually facilitate inflammation, through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor (TNF)-alpha and CRP production. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression and atherosclerosis. Better understanding of the neuroendocrine control of inflammation may provide critical insights into mechanisms underlying a variety of common human immune-related diseases.
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PMID:Neurohormonal-cytokine interactions: implications for inflammation, common human diseases and well-being. 1771 84

The objectives of the present study were to evaluate the presence of antipolymer antibody (APA) seropositivity in 285 Italian patients affected by primary fibromyalgia (FM) and to verify whether APA levels correlate with disease severity and with cytokine levels.APA levels were determined on serum samples by an indirect ELISA kit that detects IgG APA. Cytokines (IL-1, IL-6, IL-8, IL-10 and TNFalpha) were measured by ELISA in plasma. The impact of FM on the quality of life was estimated using the Fibromyalgia Impact Questionnaire, while pain severity was evaluated using a visual analogic scale. Patients were also characterized by the presence of tiredness, stiffness, nonrestorative sleep, anxiety, depression, tension headache, irritable bowel syndrome, temporomandibular dysfunction and Raynaud's phenomena. Using a cut-off value of 30 U, APA-positive values were detected in 60 FM patients (21.05%) and in 15 healthy control individuals (15.00%) without significant differences among their levels or the percentage of seropositivity. FM patients with moderate and severe symptoms had slightly higher APA levels with respect to patients with mild symptoms. APA-seropositive patients exhibited significant correlations between APA levels and the Fibromyalgia Impact Questionnaire estimate (P = 0.042), tiredness (P = 0.003) and IL-1 levels (P = 0.0072). In conclusion, APA cannot be considered a marker of disease in Italian FM patients. The presence of APA, however, might permit the identification of a subset of FM patients with more severe symptoms and of patients who may respond differently to different therapeutic strategies.
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PMID:Antipolymer antibody in Italian fibromyalgic patients. 1782 28

Complex regional pain syndromes (CRPS) are characterized by persistent and severe pain after trauma or surgery. Neuro-immune alterations are assumed to play a pathophysiological role. Here we set out to investigate whether patients with CRPS have altered systemic pro- and anti-inflammatory cytokine profiles compared to controls on mRNA and protein level. We studied blood cytokine mRNA and protein levels of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF), interleukin-2 (IL-2) and IL-8 and the anti-inflammatory cytokines IL-4, IL-10, and transforming growth factor-beta1 (TGF beta 1) in 40 prospectively recruited patients with CRPS I, two patients with CRPS II, and 34 controls. Quantitative real-time PCR and enzyme linked immunosorbent assay were used. Additionally, the patients underwent quantitative sensory testing and were assessed with the McGill pain questionnaire and the Hospital anxiety and depression scale. Patients with CRPS had higher blood TNF and IL-2 mRNA levels (p=0.005; p=0.04) and lower IL-8 mRNA levels (p<0.001) than controls. The mRNA for the anti-inflammatory cytokines IL-4 and IL-10 was reduced in the patient group (p=0.004; p=0.006), whereas TGF beta 1 mRNA levels did not differ between groups. These results were paralleled by serum protein levels, except for TGF beta 1, which was reduced in patients with CRPS, and for IL-8, which gave similar protein values in both groups. Sensory testing showed a predominant loss of small fiber-related modalities in the patient group. The shift towards a pro-inflammatory cytokine profile in patients with CRPS suggests a potential pathogenic role in the generation of pain.
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PMID:Differential expression patterns of cytokines in complex regional pain syndrome. 1789 83

Cytokines such as angiogenin (ANG) and interleukin (IL-8) have been shown to be related to depressive symptoms and inflammatory diseases like coronary heart disease. They may thus be used as stress biomarkers to identify and prevent health problems. To investigate the relationship between cytokines and nurses' job-related stress, levels of urinary ANG and IL-8 were measured in healthy female hospital nurses in Japan. The level of job-related stress of the subjects was evaluated using the Nursing Stress Scale (NSS), with the participants being classified into high- or low-stress groups for each subscale according to their scores. The participants' subjective psychological states were assessed using the Profile of Mood States--Short Form Japanese version (POMS-SFJ). Urinary ANG, IL-8, and cortisol levels and subjective psychological states for two groups were compared for each NSS subscale. The fatigue and depression scores of POMS-SFJ subscales in the present study were higher than those of the general healthy Japanese population. Based on the mean score of the combined participants, nurses were experiencing the highest stress related to the pressure of having responsibility for patients' life support care (PPLC). Nurses reporting high levels of stress related to PPLC and conflict with physicians had high levels of urinary ANG. Urinary ANG levels may thus be associated with high levels of job stress.
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PMID:The relationship between job stress and urinary cytokines in healthy nurses: a cross-sectional study. 1882

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