UNIPROT:P05231 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The evolution of nasal inflammation during a common cold in patients with nasal polyposis under topical steroid treatment is not clearly defined in the literature. Objective of this study was to analyse nasal inflammation during a common cold in patients with nasal polyposis under topical steroid treatment in comparison with control subjects. Two groups of subjects (35 consecutive patients with nasal polyposis receiving medical treatment, and 17 control subjects without any symptoms of chronic rhino-sinusitis) were studied: 10 patients with nasal polyposis and 11 controls had a common cold during a one-year follow-up period. Nasal lavage was performed at baseline and during the common cold. Soluble inflammatory mediators and permeability markers were determined in the nasal lavage fluid, as well as total and differential counts of the cells present. At baseline, no significant difference between controls and patients was observed, except for eosinophils. Paired comparisons between baseline and cold in controls revealed that all measured parameters, except for eosinophils, increased in the second nasal lavage. In nasal polyposis patients, the total cell neutrophil counts tended to increase. However, most of the concentrations of soluble parameters did not vary significantly in the second lavage, except for interleukin-6. In conclusion nasal inflammation markers appear to be similar in patients with and without nasal polyposis during a common cold when nasal polyposis patients are under topical steroid treatment.
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PMID:Nasal inflammation induced by a common cold: comparison between controls and patients with nasal polyposis under topical steroid therapy. 1760 35

Coronary endothelial function is impaired in hypertension; however, the severity of this impairment varies among patients. We aimed to identify the predictors of coronary endothelial dysfunction among clinical variables related to hypertension and atherosclerosis. Twenty-seven untreated, uncomplicated essential hypertensive patients and 10 age-matched healthy controls were studied prospectively. Myocardial blood flow (MBF) was measured by using (15)O-water positron emission tomography (PET) at rest and during a cold pressor test (CPT). Coronary vascular resistance (CVR) during CPT was used as a marker of coronary endothelial function. Serum low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, malondialdehyde-LDL, homeostasis model assessment, high-sensitivity C-reactive protein (hs-CRP), and plasma interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha were also measured. CVR during CPT was significantly higher in hypertensive patients than in healthy controls (114+/-26 vs. 94+/-12 mmHg/[mL/g/min]; p<0.05). By univariate analysis, CVR during CPT was correlated with LDL cholesterol (r=0.38, p<0.05), IL-6 (r=0.46, p<0.02), and TNF-alpha (r=0.39, p<0.05) in hypertensive patients. By multivariate analysis, IL-6 and TNF-alpha were significant independent predictors of CVR during CPT. Elevated plasma IL-6 and TNF-alpha levels were independent predictors of coronary endothelial dysfunction in hypertensive patients. These results suggest that plasma IL-6 and TNF-alpha might be useful for identifying the high risk subgroup of hypertensive patients with coronary endothelial dysfunction and provide an important clue to link systemic inflammation to the development of coronary atherosclerosis.
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PMID:Plasma interleukin-6 and tumor necrosis factor-alpha can predict coronary endothelial dysfunction in hypertensive patients. 1766 58

In this study, we wished to determine whether the changes in metabolism observed during exercise in the cold are associated with changes in interleukin-6 (IL-6) and/or its soluble receptors. Eight healthy male participants performed 1 h of cycling exercise at 70% VO2max in a control (20 degrees C) and cold (0 degrees C) environment. Plasma concentrations of IL-6, soluble IL-6 receptor (sIL-6R), and sgp130 were measured before exercise, at 30 and 60 min of exercise, and 60 min after exercise. Substrate oxidation was estimated through measures of pulmonary gas exchange recorded between 50 and 55 min of cycling. Exercise in the cold resulted in an increase (P < 0.05) in carbohydrate oxidation (mean 2.58 g.min(-1), s = 0.49 at 20 degrees C vs. 2.85 g.min(-1), s = 0.58 at 0 degrees C) and a decrease (P < 0.05) in fat oxidation (0.55 g.min(-1), s = 0.17 at 20 degrees C vs. 0.38 g.min(-1), s = 0.16 at 0 degrees C) compared with the control trial. Interleukin-6 concentrations were elevated (P < 0.05) after 60 min of exercise in both the cold and control trials, with no differences between trials at any instant. Neither sIL-6R nor sgp130 was affected by exercise or the environment. The alterations in carbohydrate and fat utilization during 1 h of exercise in the cold are not paralleled by changes in plasma concentrations of IL-6 or its soluble receptors.
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PMID:The response of plasma interleukin-6 and its soluble receptors to exercise in the cold in humans. 1856 58

Catastrophizing exerts its deleterious effects on pain via multiple pathways, and some researchers have reported that high levels of catastrophizing are associated with enhanced physiological reactivity to painful stimulation. In this project, 42 generally healthy adults underwent a series of psychophysical pain testing procedures assessing responses to noxious mechanical, heat, and cold stimuli. Pain catastrophizing cognitions were assessed prior to and then immediately after the various pain induction procedures. Blood samples were taken at baseline and then at several time points from the end of the procedures to 1h post-testing. Samples were assayed for serum levels of cortisol and interleukin-6 (IL-6). Both cortisol and IL-6 increased from baseline during the post-testing period (p's<.05), with cortisol returning to baseline by 1h post-testing and IL-6 remaining elevated. Pain catastrophizing, measured immediately after the pain procedures, was unrelated to cortisol reactivity, but was strongly related to IL-6 reactivity (p<.01), with higher levels of catastrophizing predicting greater IL-6 reactivity. In multivariate analyses, the relationship between catastrophizing and IL-6 reactivity was independent of pain ratings. Collectively, these findings suggest that cognitive and emotional responses during the experience of pain can shape pro-inflammatory immune system responses to noxious stimulation. This pathway may represent one important mechanism by which catastrophizing and other psychosocial factors shape the experience of both acute and chronic pain in a variety of settings.
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PMID:Association of catastrophizing with interleukin-6 responses to acute pain. 1877 95

Respiratory syncytial virus (RSV) is a common cause of infection that is associated with a range of respiratory illnesses, from common cold-like symptoms to serious lower respiratory tract illnesses such as pneumonia and bronchiolitis. RSV is the single most important cause of serious lower respiratory tract illness in children <1 year of age. Host innate and acquired immune responses activated following RSV infection have been suspected to contribute to RSV disease. Toll-like receptors (TLRs) activate innate and acquired immunity and are candidates for playing key roles in the host immune response to RSV. Leukocytes express TLRs, including TLR2, TLR6, TLR3, TLR4, and TLR7, that can interact with RSV and promote immune responses following infection. Using knockout mice, we have demonstrated that TLR2 and TLR6 signaling in leukocytes can activate innate immunity against RSV by promoting tumor necrosis factor alpha, interleukin-6, CCL2 (monocyte chemoattractant protein 1), and CCL5 (RANTES). As previously noted, TLR4 also contributes to cytokine activation (L. M. Haynes, D. D. Moore, E. A. Kurt-Jones, R. W. Finberg, L. J. Anderson, and R. A. Tripp, J. Virol. 75:10730-10737, 2001, and E. A. Kurt-Jones, L. Popova, L. Kwinn, L. M. Haynes, L. P. Jones, R. A. Tripp, E. E. Walsh, M. W. Freeman, D. T. Golenbock, L. J. Anderson, and R. W. Finberg, Nat. Immunol. 1:398-401, 2000). Furthermore, we demonstrated that signals generated following TLR2 and TLR6 activation were important for controlling viral replication in vivo. Additionally, TLR2 interactions with RSV promoted neutrophil migration and dendritic cell activation within the lung. Collectively, these studies indicate that TLR2 is involved in RSV recognition and subsequent innate immune activation.
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PMID:Respiratory syncytial virus activates innate immunity through Toll-like receptor 2. 1901 63

Numerous Echinacea preparations are available on the market for the prevention and treatment of cold and 'flu symptoms and inflammatory conditions associated with infections. Most of these preparations are consumed orally in the form of aqueous or ethanol extracts and tinctures. Since the recommended consumption normally involves a brief local exposure to the diluted preparation at an unspecified time in relation to the actual infection, then it is important that experimental models for the evaluation of Echinacea reflect these limitations. A line of human bronchial epithelial cells, in which rhinoviruses stimulate the production of pro-inflammatory cytokines, was used to evaluate several relevant parameters. The chemically characterized Echinacea preparation (Echinaforce) was capable of inhibiting completely the rhinovirus induced secretion of IL-6 (interleukin-6) and IL-8 (chemokine CXCL-8) in these cells, regardless of whether the Echinacea was added before or after virus infection, and in response to a range of virus doses. This inhibitory effect was also manifest under conditions resembling normal consumption with respect to the duration of exposure to Echinacea and the Echinacea dilution. It is concluded that under real life conditions of Echinacea consumption, the virus-induced stimulation of pro-inflammatory cytokines can be effectively reversed or alleviated.
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PMID:Echinacea as an antiinflammatory agent: the influence of physiologically relevant parameters. 1910 35

Vitamin B(6) may lower risk of colorectal cancer by preventing aberrations in one-carbon metabolism or by anti-inflammatory effects. We prospectively evaluated the association between plasma levels of pyridoxal 5'-phosphate (PLP; the active form of vitamin B(6)) and risk of colorectal cancer in a nested case-control study within the Physicians' Health Study. Among 14,916 men who provided blood specimens in 1982 to 1984, we identified 197 incident colorectal cancer cases through 2000 and individually matched them to 371 controls by age and smoking status. Plasma PLP levels were positively correlated with cold cereal intake and plasma levels of folate and vitamin B(12) (age- and smoking-adjusted partial correction r = 0.28-0.48) and slightly inversely correlated with body mass index (r = -0.11) and plasma levels of homocysteine, C-reactive protein, tumor necrosis factor-alpha receptor 2, and interleukin-6 (r = -0.23 to -0.14). With control for these factors and known risk factors for colorectal cancer, plasma PLP levels were significantly inversely associated with risk of colorectal cancer; compared with men in the lowest quartile, those with PLP in quartiles 2 to 4 had relative risks (95% confidence interval) of 0.92 (0.55-1.56), 0.42 (0.23-0.75), and 0.49 (0.26-0.92; P(trend) = 0.01), respectively. In conclusion, vitamin B(6) may protect against colorectal cancer independent of other one-carbon metabolites and inflammatory biomarkers.
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PMID:Prospective study of plasma vitamin B6 and risk of colorectal cancer in men. 1933 55

Renal ischemia/reperfusion (I/R) is characterized by severe inflammatory damage. We assessed the effect of administrating recently developed nitrosothiol compounds acting as nitric oxide (NO) donors on the production of cytokines and other markers of acute inflammatory reaction in an experimental model of warm (I/R), and in a model of cold ischemia and transplant in rats. Warm ischemia was achieved by ligation of left renal pedicle for 60 min, followed by contralateral nephrectomy. NO-donors LA-803, LA-807, LA-810 were administered i.v. (1.8 micromol/kg) during 30 min before reperfusion. Cold ischemia was achieved by preservating the kidney for 24 h in Euro Collins and grafting it in consanguineous Fisher 344/Ico rats. LA-803 was administered in the preservation fluid and in the recipient rat. Reperfusion time was 4 h in warm ischemia and 3 h in cold ischemia + transplantation. Administration of LA-803, LA-807 and, in a lower proportion, LA-810 prevented from the enhanced production of tumor necrosis factor (TNF), interferon-gamma (IFN-gamma), and interleukin-1beta (IL-1beta), the decrease in interleukin-6 (IL-6) and interleukin-10 (IL-10), the increase in tissue level of superoxide anion (SOA) and superoxide dismutase (SOD), and the increase in neutrophil infiltration induced by warm I/R. Treatment with LA-803 in animals with renal transplantation after cold ischemia was also associated with reduced plasma levels of TNF, IFN-gamma, and IL-1beta, increased plasma levels of IL-6 and IL-10, reduced renal levels of SOA and SOD, and reduced neutrophil infiltration. These data demonstrate that systemic administration of new NO-donors with nitrosothiol structure diminished inflammatory responses in a kidney subjected to warm I/R or cold ischemia and transplantation.
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PMID:Protective effect of new nitrosothiols on the early inflammatory response to kidney ischemia/reperfusion and transplantation in rats. 1951 43

The immunomodulatory effects of Korean mistletoe lectin (KML), one of the major active components in Viscum album L. var. coloratum, were investigated in vitro in immune cell proliferation and natural killer (NK) cell- and macrophage-mediated cytotoxicity, and in vivo in the forced swim test and cold stress. In mitogen-induced lymphocyte proliferation of murine splenocytes, concanavalin A and lipopolysaccharide significantly increased the proliferation of T cell and B cell lymphocytes, respectively. KML exposure increased lymphocyte proliferation in response to mitogen. KML also increased the splenic NK cell and macrophage activities in vitro. Exposure to KML increased production of cytokines such as interleukin-1 and interleukin-6 by macrophages. Two-week treatment with KML (30, 100, 300 and 600 microg/kg) increased the recruitment of lymphocytes, monocytes and macrophages. In the forced swim test, the immobility time was significantly attenuated by treatment with KML (300 and 600 microg/kg). In a cold stress experiment, spleen and thymus weight increased in KML-treated mice, while the weight of adrenal gland was lower than that in vehicle-treated mice. The levels of serum aminotransferases, lactate dehydrogenase and alkaline phosphatase were decreased by KML treatment. KML treatment also induced increases in the percentages of CD4(+) and CD8(+) cells in thymus. Our results suggest that KML enhances the immune system through modulation of lymphocytes, NK cells, and macrophages.
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PMID:Immunomodulating effects of Korean mistletoe lectin in vitro and in vivo. 1978 34

The current study investigated the effects of a pre-cooling intervention on physiological and performance responses to team-sport training in the heat. Seven male lacrosse players performed a familiarization session and 2 randomized, counterbalanced sessions consisting of a 30-minute intermittent-sprint conditioning session. Prior to the sessions, players performed a 20-minute mixed-method, part-body cooling intervention (consisting of cooling vests, cold towels to the neck, and ice packs to the quadriceps) or no cooling intervention. Performance was determined from collection of 1 Hz global positioning system (GPS) data and analyzed for distance and speed. Prior to, during, and following the sessions, core temperature, heart rate, rating of perceived exertion (RPE), and thermal sensation scale (TSS) were measured; additionally, a venous blood sample was collected before and after each session for measurement of interleukin-6 (IL-6), insulin-like growth factor (IGF-1) and insulin-like growth factor-binding protein3 (IGF-BP3). Results indicated that a greater distance was covered during the pre-cooling condition (3.35 +/- 0.20 vs. 3.11 +/- 0.13 km; p = 0.05). Further, most of this improvement was evident from a greater distance covered during moderate intensities of 7 to 14 km/h (2.28 +/- 0.18 vs. 2.00 +/- 0.24 km; p = 0.05). Peak speeds and very-high-intensity efforts (20 km/h +/-) were not different between conditions (p > 0.05). The increase in core temperature was blunted following cooling, with a lower core temperature throughout the cooling session (38.8 +/- 0.3 vs. 39.3 +/- 0.4 degrees C; p < 0.05). However, there were no differences in heart rate, RPE, TSS, IL-6, IGF-1, or IGF-BP3 between conditions (p > 0.05). Accordingly, the use of a mixed-method, part-body cooling intervention prior to an intermittent-sprint training session in the heat can assist in reducing thermoregulatory load and improve aspects of training performance for team sports.
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PMID:The use of mixed-method, part-body pre-cooling procedures for team-sport athletes training in the heat. 1991 Aug 21

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