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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute mental stress may contribute to atherosclerosis by affecting inflammation and coagulation; however, the crosstalk between inflammation and coagulation during stress has not been studied. In the present study, we investigated the association of plasma fibrinogen, plasma IL-6 (interleukin-6) and free salivary cortisol with the procoagulant marker D-dimer reflecting fibrin formation both over a 2-h period and in response to acute mental stress. Twenty-one male volunteers (mean age, 47+/-8 years) underwent the Trier Social Stress Test combining a 3-min preparation phase, a 5-min job interview and 5-min mental arithmetic test before an audience. IL-6, fibrinogen, D-dimer and cortisol were measured immediately before and after stress, and after 45 min and 105 min of recovery from stress. Two distinct areas under the curve were computed to obtain integrated measures of total protein activity over the entire 2-h period and of stress reactivity of proteins. IL-6 (P < 0.001), fibrinogen (P = 0.001), D-dimer (P = 0.021) and cortisol (P < 0.001) had all significantly changed across the four time points assessed, as determined by ANOVA. For the entire 2-h period, total fibrinogen activity (R2 = 0.33, P = 0.007) and total cortisol activity (DeltaR2 = 0.17, P = 0.034) explained 50% of the variance in total D-dimer activity. Stress-induced changes in fibrinogen (R2 = 0.47, P = 0.001) and IL-6 (DeltaR2 = 0.18, P = 0.008) together explained 65% of the variance in D-dimer reactivity to stress. Total fibrin formation was independently predicted by fibrinogen and hypothalamo-pituitary-adrenal activity. Pro-inflammatory and procoagulant changes with stress were associated. Aside from fibrinogen reactivity, IL-6 reactivity was an independent predictor of stress-induced fibrin formation.
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PMID:Different contribution of interleukin-6 and cortisol activity to total plasma fibrin concentration and to acute mental stress-induced fibrin formation. 1575 67

Animal studies have shown that an acute stressor in close temporal proximity to immune challenge can enhance the response to delayed-type hypersensitivity and antibody response to vaccination. The current study examined the effects of acute exercise or mental stress prior to influenza vaccination on the subsequent antibody response to each of the three viral strains. Sixty young healthy adults (31 men, 29 women) were randomly allocated to one of three task conditions: dynamic exercise, mental stress, or control. After an initial baseline, participants completed their allocated 45 min task and then received the influenza vaccine. Plasma cortisol and interleukin-6 were determined at the end of baseline, after the task, and after 60 min recovery. Antibody titres were measured pre-vaccination and at 4 weeks and 20 weeks post-vaccination follow-ups. For the A/Panama strain, women in both the exercise and mental stress conditions showed higher antibody titres at both 4 and 20 weeks than those in the control condition, while men responded similarly in all conditions. Interleukin-6 at +60 min recovery was found to be a significant predictor of subsequent A/Panama antibody response in women. In line with animal research, the current study provides preliminary evidence that acute stress can enhance the antibody response to vaccination in humans.
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PMID:Acute stress exposure prior to influenza vaccination enhances antibody response in women. 1610 36

The pathophysiological mechanisms underlying the association between psychological stress and cardiovascular disease are unclear. Interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) are inflammatory cytokines playing a pivotal role in atherosclerosis. IL-1beta activates IL-6, and both cytokines are produced by peripheral blood mononuclear cells. One mechanism through which stress could promote atherosclerosis is by regulating mononuclear cell cytokine gene expression. We studied cardiovascular and cytokine responses in 32 healthy men participating in two 5-min mental tasks and in 10 controls. Blood pressure and heart rate, assessed using a Portapres-2, increased significantly following tasks in all participants. Plasma IL-6 levels, determined by ELISA, also increased following tasks, with maximum levels detected 2h post-stress. Quantitative RT-PCR analysis showed that mononuclear cell IL-1beta gene expression rose significantly at 30 min post-stress and remained elevated at 75 and 120 min. Increases in IL-1beta gene expression correlated positively with plasma IL-6 responses, cardiovascular responses, subjective stress ratings, and anxiety symptoms. No changes were detected in controls. Stress-induced activation of mononuclear IL-1beta is a novel mechanism potentially linking stress and heart disease. This mechanism could also play a role in other inflammatory diseases exacerbated by stress.
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PMID:Psychological stress activates interleukin-1beta gene expression in human mononuclear cells. 1621 25

Biochemical markers of inflammation have been used in recent physical activity intervention studies. However, these same biochemical markers, mainly proinflammatory cytokines, may also be influenced by the individual's level of stress and mood. Accordingly, this pilot study was implemented to determine the effect of a physical activity intervention on perceived stress, mood, quality of life, serum interleukin-6 (IL-6), and cortisol among 10 older adults, age 60 to 90. The results were compared to those of 10 older adults who were not engaging in regular physical activity. The 10-week intervention was applied using student nurses who taught the older adults how to calculate 60% of their maximum heart rate while ambulating for 30-min intervals. After the 10-week period, the participants in the exercise group reported significant improvements in stress, mood, and several quality of life indices. They also demonstrated a significant decrease in serum IL-6. Stress, mood, and quality of life scores in the exercise group were also significantly improved compared to the control group. This study adds information on the specific intensity, duration, and frequency of exercise necessary to achieve improvements in psychological variables and IL-6 levels. It also supports the need to measure psychological stress in physical activity intervention studies. Although the psychological variables were highly correlated, there were only weak correlations found with IL-6, suggesting that other factors are likely involved in reducing IL-6 when engaging in low-impact physical activity.
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PMID:The effects of exercise on perceived stress and IL-6 levels among older adults. 1717 17

Cytokines are pleiotropic substances that are known to participate in inflammatory and immune responses as well as cell differentiation and proliferation. Interleukin-6 (IL-6) is a key cytokine with pro-inflammatory function. Wound healing is a complex cascade of physiologic events comprising inflammation, proliferation and remodeling, and proceeds with the integrated actions of different cells, cytokines, and the extracellular matrix. Aberrant wound healing results in keloid formation which causes disfigured appearance, discomfort, psychological stress, and patient frustration. In this review, the role of IL-6 signaling pathway in the pathogenesis of keloid is assessed and its potential as a therapeutic target is addressed. The existing data suggest that IL-6 mediated inflammation is a key player and may be considered as a common causative factor for development of keloid. Furthermore, in a recent comprehensive study, we confirmed the functional role of IL-6 signaling in keloid pathogenesis. Accordingly, inhibitory strategies of IL-6 signaling pathway by targeting the IL-6 receptors, its downstream effecters, or other molecules influencing this pathway appear to have considerable potential as new therapeutic or preventive challenges for keloid. Hopefully, several IL-6 blocking agents including a humanized antibody to IL-6 receptor have been developed and successfully used in clinical trials of inflammatory diseases. It is likely that these agents may prove worthy in the treatment or prevention of keloid as well. Future in-depth exploration of such challenges will shed light on their efficacy and safety for clinical application in keloid.
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PMID:Essential role of IL-6 signaling pathway in keloid pathogenesis. 1738 73

Physical and mental stressors result in increased inflammation markers in populations free of coronary artery disease (CAD). However, inflammatory responses to mental and exercise challenges have not been established in patients with CAD. This study investigated the responses of inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1, in patients with CAD after successful elective percutaneous coronary intervention (n = 36, 59 +/- 8 years of age, 33% women) and healthy controls without a history of CAD (n = 28, 54 +/- 10 years of age, 36% women). Increases in inflammatory markers were examined in response to mental challenge tasks (anger recall and mental arithmetic) and treadmill exercise. Stress echocardiography was used to rule out stress-induced ischemia as a possible confounding factor. Results showed that CRP increased significantly to mental challenge and exercise (p values <0.01), and CRP responses were higher in patients with CAD than in controls (change in mental arithmetic 0.19 +/- 0.11 vs 0.01 +/- 0.03 mg/L, p = 0.003; change in exercise 0.57 +/- 0.11 vs 0.08 +/- 0.0.03 mg/L, p = 0.001). Increased norepinephrine responses were related to larger CRP and IL-6 increases to mental challenge tasks (p values <0.05). Exercise elicited increased CRP, IL-6, and soluble intercellular adhesion molecule-1 levels (p values <0.01), and these responses were larger than with mental challenge tasks (p values <0.05). In conclusion, mental stress and exercise induce increased levels of inflammatory markers in patients with CAD. These stress-induced increases are larger than in healthy subjects, occur in the absence of myocardial ischemia, and are related to the neurohormonal stress response.
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PMID:Effects of acute mental stress and exercise on inflammatory markers in patients with coronary artery disease and healthy controls. 1832 37

Anemia is a widespread public health problem. The psychological stress decreases serum iron level and inhibits erythropoiesis. However, the molecular mechanisms involved, leading to iron mal-regulation are not well known. We used a communication box paradigm to induce psychological stress and found that serum iron level decreased after 3d while liver iron storage increased after 7d. Moreover, psychological stress up-regulated expressions of interleukin-6 (IL-6) and hepcidin, while down-regulating ferroportin expression after 3d. These changes were blocked by the injection of IL-6 monoclonal antibody. In conclusion, the IL-6-hepcidin axis is up-regulated by psychological stress in rats, resulting in hypoferremia and increase of hepatic iron storage.
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PMID:Psychological stress induces hypoferremia through the IL-6-hepcidin axis in rats. 1854 Nov 41

Acute mental stress tests have helped to clarify the pathways through which psychosocial factors are linked to disease risk. This methodology is now being used to investigate potentially protective psychosocial factors. We investigated whether global self-esteem might buffer cardiovascular and inflammatory responses to acute stress. One hundred and one students completed the Rosenberg Self-Esteem Scale. Heart rate and heart rate variability (HRV) were recorded for 5 min periods at baseline, during two mental stress tasks, (a speech and a color-word task) and 10, 25 and 40 min into a recovery period. Plasma levels of tumor-necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL-1Ra) were assessed at baseline, immediately post-stress and after 45 min recovery. Repeated measures analysis of variance demonstrated that heart rate levels were lower across all time points in those with high self-esteem, although heart rate reactivity to stress was not related to self-esteem. There were no differences in baseline HRV, TNF-alpha, IL-6 or IL-1Ra. Multiple linear regressions revealed that greater self-esteem was associated with a smaller reduction in heart rate variability during the speech task, but not the color-word task. Greater self-esteem was associated with smaller TNF-alpha and IL-1Ra responses immediately following acute stress and smaller IL-1Ra responses at 45 min post-stress. In conclusion, global self-esteem is associated with lower heart rate and attenuated HRV and inflammatory responses to acute stress. These responses could be processes through which self-esteem protects against the development of disease.
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PMID:Self-esteem levels and cardiovascular and inflammatory responses to acute stress. 1864 32

Obesity is associated with an elevated risk of hypertension and cardiovascular disease. The adipocyte hormone leptin, which stimulates energy expenditure in animals by activating the sympathetic nervous system (SNS), is believed to play a role in this association. However, evidence in humans remains sparse. We investigated the relationship between circulating leptin and cardiovascular and inflammatory responses to acute psychological stress in humans. Participants were 32 men and 62 women aged 18-25 years. Cardiovascular activity was assessed using impedance cardiography at baseline, during acute laboratory stress, and during a 45-min recovery period. Plasma cytokines were measured in blood drawn at baseline and 45-min poststress. In women only, baseline plasma leptin was significantly associated with stress-induced changes in heart rate (beta = 0.53, P = 0.006), heart rate variability (HRV) (beta = -0.44, P = 0.015), and cardiac preejection period (PEP) (beta = -0.51, P = 0.004), independent of age, adiposity, and smoking. Women's plasma leptin levels also correlated with stress-induced elevations in the proinflammatory cytokine interleukin-6 (IL-6) (beta = 0.35, P = 0.042). Circulating leptin is an independent predictor of sympathetic cardiovascular activity, parasympathetic withdrawal, and inflammatory responses to stress in women. Because cardiovascular and inflammatory stress responses are predictive of future cardiovascular disease, leptin may be a mechanism mediating the adverse effects of stress and obesity on women's cardiovascular health.
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PMID:Circulating leptin and stress-induced cardiovascular activity in humans. 1882 Jun 49

Activation of the innate immune system is commonly accompanied by a set of behavioural, psychological and physiological changes known as 'sickness behaviour'. In animals, infection-related sickness symptoms are significantly increased by exposure to psychosocial stress, suggesting that psychological and immune stressors may operate through similar pathways to induce sickness. We used a double-blind, randomised, placebo-controlled design to examine the effect of acute psychological stress on immune and subjective mood responses to typhoid vaccination in 59 men. Volunteers were assigned to one of four experimental conditions in which they were either injected with typhoid vaccine or saline placebo, and then either rested or completed two challenging behavioural tasks. Typhoid vaccine induced a significant rise in participants' serum levels of interleukin-6 (IL-6) and this response was significantly larger in the stress versus rest conditions. Negative mood increased immediately post-tasks, an effect also more pronounced in the vaccine/stress condition. In the vaccine/stress group, participants with larger IL-6 responses had heightened systolic blood pressure responses to tasks and elevated post-stress salivary levels of the noradrenaline metabolite 3-methoxy-phenyl glycol (MHPG) and cortisol. Our findings suggest that, as seen in animals, psychological and immune stressors may act synergistically to promote inflammation and sickness behaviour in humans.
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PMID:Synergistic effects of psychological and immune stressors on inflammatory cytokine and sickness responses in humans. 1883 37


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