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 systemic inflammatory response to cardiopulmonary bypass (CPB) is associated with increased production of cytokines. This systemic inflammatory response characterized by the activation of interleukin-6 (IL-6) and interleukin-8 (IL-8) during and after CPB is well documented. A prospective, randomized, double-blind study was performed so as to understand the effects of low-dose methyl prednisolone sodium succinate (MPSS) on the circulating levels of serum cytokines and clinical outcome. Twenty patients were randomly divided into two groups on the basis of the administration of low-dose (1 mg/kg) MPSS (n = 10) and placebo (n = 10) into the pump prime solution. All patients were scheduled to undergo a primary elective coronary artery bypass grafting operation. Patients receiving concurrent corticosteroids, salicylates, dipyridamol or anticoagulants were excluded from the study. Other exclusion criteria were concurrent chronic obstructive pulmonary disease, chronic renal failure, insulin-dependent diabetes, congestive cardiac failure, peptic ulcer history, prior cardiac operations, recent (in a one-month period) myocardial infarction and steroid dependency. Mild systemic hypothermia (30-32 degrees C, rectal) was assured during the CPB. Four blood samples were drawn from the radial artery catheter immediately before starting CPB (T1), following protamine administration (T2) and at 24 (T3) and 48 h (T4) after completion of CPB. In each sample, creatine kinase-myocardial band (CK-MB), white blood cell (WBC), IL-6 and IL-8 levels were measured. IL-6 and IL-8 concentrations were measured by enzyme immunoassay and enzyme-linked immunoabsorbant assay methods. Serum IL-6 T2 and serum IL-6 T3 levels were significantly higher than IL-6 T1 levels in both groups (p < 0.001) and (p < 0.01), and there was no significant elevation in serum IL-8 levels in either group. Serum IL-6 levels were significantly higher in the placebo group than in the MPSS group at T3 (p < 0.009). There was no significant difference in CK-MB T1 levels between the groups. Although there was no significant difference between CK-MB T1 and T2 levels in the MPSS group, the CK-MB T2 and CK-MB T3 levels were significantly higher than T1 levels in the placebo group (p < 0.001) and (p < 0.05). There was significant elevation of WBC levels at T2 and T3 in both groups without notable difference between the groups (p < 0.05). This study has shown that low-dose MPSS suppresses CPB-induced inflammatory response. Further clinical studies (on larger and higher risk groups) may reveal more information on relations between morbidity and cytokine levels which may have some predictive value on clinical outcome following CPB.
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PMID:Effect of low-dose methyl prednisolone on serum cytokine levels following extracorporeal circulation. 1041 Dec 50

Common colds are associated with exacerbations of chronic obstructive pulmonary disease (COPD). However, the role of the common cold virus (human rhinovirus) in the production of symptoms and lower airway inflammation at COPD exacerbation is unknown. Thirty three patients with moderate-to-severe COPD were seen at baseline, when the number of chest infections in the previous year was noted, and acutely at COPD exacerbation. Within 48 h after the onset of the exacerbation and at baseline, nasal aspirates and induced sputum were taken for rhinovirus reverse transcriptase polymerase chain reaction (RT-PCR) analysis and determination of cytokine levels. Symptoms, recorded on diary cards, were noted and forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured. At exacerbation, mean FEV1 and FVC fell significantly from baseline (p<0.001). Ten of 43 exacerbations were associated with rhinovirus infection, detected in induced sputum. In four of these, nasopharyngeal samples contained no detectable rhinovirus. All baseline samples were negative for rhinovirus. The simultaneous presence of increased nasal discharge/nasal congestion (in 26 of the 43 exacerbations) and increased sputum (29 exacerbations) was strongly associated with the presence of rhinovirus (odds ratio 6.15; p=0.036). Total symptom scores were greater for rhinovirus as compared to nonrhinovirus exacerbations (p=0.039). Median baseline sputum interleukin-6 levels rose from 90.2 to 140.3 pg x mL(-1) at exacerbation (p=0.005); the change was greater in the presence of rhinovirus infection (p=0.008). Rhinovirus infection can be detected at chronic obstructive pulmonary disease exacerbation. This is associated with elevation of lower airway interleukin-6 levels, which may mediate lower airway symptom expression during chronic obstructive pulmonary disease exacerbations.
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PMID:Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease. 1110 12

The effects of respiratory viral infection on the time course of chronic obstructive pulmonary disease (COPD) exacerbation were examined by monitoring changes in systemic inflammatory markers in stable COPD and at exacerbation. Eighty-three patients with COPD (mean [SD] age, 66.6 [7.1] yr, FEV(1), 1.06 [0.61] L) recorded daily peak expiratory flow rate and any increases in respiratory symptoms. Nasal samples and blood were taken for respiratory virus detection by culture, polymerase chain reaction, and serology, and plasma fibrinogen and serum interleukin-6 (IL-6) were determined at stable baseline and exacerbation. Sixty-four percent of exacerbations were associated with a cold occurring up to 18 d before exacerbation. Seventy-seven viruses (39 [58.2%] rhinoviruses) were detected in 66 (39.2%) of 168 COPD exacerbations in 53 (64%) patients. Viral exacerbations were associated with frequent exacerbators, colds with increased dyspnea, a higher total symptom count at presentation, a longer median symptom recovery period of 13 d, and a tendency toward higher plasma fibrinogen and serum IL-6 levels. Non-respiratory syncytial virus (RSV) respiratory viruses were detected in 11 (16%), and RSV in 16 (23.5%), of 68 stable COPD patients, with RSV detection associated with higher inflammatory marker levels. Respiratory virus infections are associated with more severe and frequent exacerbations, and may cause chronic infection in COPD. Prevention and early treatment of viral infections may lead to a decreased exacerbation frequency and morbidity associated with COPD.
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PMID:Respiratory viruses, symptoms, and inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease. 1171 91

Some patients with COPD are prone to frequent exacerbations, which are an important determinant of health status. Such patients have elevated airway cytokine levels, suggesting the presence of increased inflammation that may increase their susceptibility to exacerbation. The inflammatory response during a COPD exacerbation is variable, but increases in interleukin-6 levels during the exacerbation are related to the presence of a common cold. Rhinovirus infection is the most important etiologic factor in COPD exacerbations and is an important target for preventive therapy. The reduction of COPD exacerbations will have an important impact on the considerable morbidity and mortality associated with COPD.
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PMID:Exacerbations: etiology and pathophysiologic mechanisms. 1201 Aug 42

The objective of this study was to determine whether high concentrations of circulating interleukin-6 (IL-6) and/or the soluble receptor of IL-6 (SRIL-6) may mediate systemic inflammatory activity in patients with alpha-1 antitrypsin deficiency (AATD). To that end we assessed serum concentrations of IL-6 and SRIL-6 for 7 patients with AATD in stable phase. The patients' mean age was 51 years (SD 5.2); mean FEV1% was 35.5% (SD 15%). IL-6 and SRIL-6 concentrations were compared with those of 23 non-AATD patients with COPD but with similar changes in lung function (mean age 63 years, SD 10.1; FEV1% 38.3%, SD 11%). The AADT patients had mean IL-6 concentrations of 4.7 pg/mL (interquartile range [IR( 4.0) and RSIL-6 levels of 129.1 ng/mL (IR 31.5). The COPD patients had IL-6 concentrations of 4.1 pg/mL (IR 4.2) and SRIL-6 levels of 140.8 ng/mL (IR 71). No significant differences between the AADT group and the COPD group were observed for either cytokine (non-parametric Mann Whitney U test, p > 0.05). Only one AADT patient had an IL-6 concentration that was higher than normal. In conclusion, the serum IL-6 and SRIL-6 concentrations of patients with AADT are not different from those of patients with COPD, similarly altered respiratory function and normal alpha-1 antitrypsin levels. These results do not point to a role for alpha-1 antitrypsin in systemic inflammatory stimulation in patients with AADT.
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PMID:[Importance of serum interleukin-6 as a mediator of systemic inflammation in patients with alpha-1 antitrypsin deficiency]. 1211 42

Cigarette smoking induces an inflammatory response in the airways that may play a key role in the pathogenesis of chronic obstructive pulmonary disease. Noninvasive markers of inflammation may, therefore, be useful in monitoring the airways of smokers as well as in the screening of subjects at high risk of developing airway obstruction. The aim of the present study was to determine whether the concentrations of the pro-inflammatory cytokine, interleukin (IL)-6, is increased in the exhaled breath condensate of smokers and whether the number of cigarettes smoked has any influence on the exhaled concentrations. The possibility that exhaled IL-6 levels are related to exhaled carbon monoxide (CO) and lung function has also been explored. Another inflammatory marker, leukotriene (LT), was also measured. Twenty-one smokers (39+/-7 yrs, 13 male) and 14 nonsmokers (45+/-6 yrs, eight male) were recruited. IL-6 and LTB4 levels in the breath condensate were measured with an immunoassay kit and exhaled CO examined by means of a modified electrochemical sensor. Higher IL-6 and exhaled CO concentrations were found in current smokers (5.6+/-1.4 pg x mL(-1) and 16.7+/-5.5 parts per million (ppm)) than in nonsmokers (2.6+/-0.2 pg x mL(-1) and 2.1+/-0.6 ppm). Elevated concentrations of LTB4 were also observed in smokers compared to nonsmokers (9.4+/-0.4 pg x mL(-1) versus 6.1+/-0.3 pg x mL(-1)). In addition, there was a correlation between IL-6 concentrations, the number of cigarettes smoked per day, exhaled CO, LTB4 and lung function. Exhaled interleukin-6 and leukotriene B4 levels may be useful noninvasive markers of airway inflammation in cigarette smokers.
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PMID:Increased inflammatory markers in the exhaled breath condensate of cigarette smokers. 1276 40

Adenosine (Ado) has been suggested to play a role in inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease. The goal of this study was to determine the effect of Ado and its receptor subtypes on cytokine release by bronchial smooth muscle cells. The A2B Ado receptor (AdoR) was expressed at the highest level among the four AdoR subtypes. Activation of the A2B AdoR by an Ado analog, 5'-(N-ethylcarboxamido)-adenosine (NECA), increased cAMP accumulation with potency (EC50 value) of 21.2 +/- 0.2 microM. The effect of NECA on the expression of the inflammatory cytokines was determined using a cDNA array consisting of 23 cytokine genes and confirmed using real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. NECA increased the release of interleukin-6 and monocyte chemotactic protein-1 proteins with EC50 values of 1.26 +/- 0.25 microM and 0.40 +/- 0.08 microM, respectively, and the maximal folds of induction were 20.8 +/- 1.7- and 6.4 +/- 0.7-fold, respectively. Selective agonists for the A1, A2A, and A3 AdoR subtypes had no effect on cytokine release. The effects of NECA were attenuated by selective antagonists of the A2B AdoR. Thus, Ado increases the release of interleukin-6 and monocyte chemotactic protein-1 from bronchial smooth muscle cells via activation of the A2B AdoR. Our findings provide a novel mechanism whereby Ado acts as a proinflammatory mediator in the airway.
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PMID:A(2B) adenosine receptors increase cytokine release by bronchial smooth muscle cells. 1285 6

Inflammatory abnormalities may be involved in the inadequate basal oxidant/antioxidant balance and local exercise-induced oxidative stress in chronic obstructive pulmonary disease (COPD) patients. The time course of oxidative stress and inflammation was investigated in 10 COPD patients and seven healthy subjects before and after local dynamic quadriceps endurance exercise at 40% of maximal strength. Venous samples were collected before, immediately after and up to 48 h after exercise. At rest, levels of an oxidant released by stimulated phagocytes, the superoxide anion, were significantly higher in patients, as were plasma levels of C-reactive protein, tumour necrosis factor-alpha and interleukin-6, inflammatory markers. An inverse relationship was found between baseline C-reactive protein levels and endurance time in patients. Six hours after exercise, superoxide anion release and levels of protein oxidation products, an index of oxidative stress, increased similarly in both groups, whereas thiobarbituric acid reactive substance levels, another index of oxidative stress, increased significantly only in patients. Plasma nonenzymatic antioxidant and inflammatory cytokine levels were unchanged by the exercise protocol. The increased baseline systemic inflammation in chronic obstructive pulmonary disease patients could be related to disturbed oxidant/antioxidant balance, and, together, these may have triggered the exercise-induced oxidative stress. The absence, however, of local exercise-induced systemic inflammation suggests that additional mechanisms explain local exercise-induced oxidative stress.
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PMID:Does systemic inflammation trigger local exercise-induced oxidative stress in COPD? 1508 51

Respiratory epithelial cells play important roles not only in host defense mechanisms, but also in inflammatory responses. Inhaled corticosteroids are widely used for the treatment of patients with inflammatory lung disorders, including asthma, chronic obstructive pulmonary disease, and sarcoidosis. Corticosteroids effectively reduce the production of inflammatory mediators, such as cytokines and chemokines. Although these molecules are also essential for host defense responses, there is no convincing evidence that inhaled corticosteroids increase susceptibility to lower respiratory tract infections. To test the involvement of Toll-like receptor (TLR) family molecules in this phenomenon, we examined the effects of various cytokines and corticosteroid on the expression of TLRs in human respiratory epithelial cells. Among the TLRs tested, TLR2 expression was significantly enhanced after stimulation with a combination of tumor necrosis factor-alpha and interferon-gamma. Dexamethasone synergistically enhanced TLR2 expression in combination with tumor necrosis factor-alpha and interferon-gamma in terms of both mRNA and protein levels. Furthermore, increased cell-surface TLR2 was functional, judging from the remarkable induction of interleukin-6, interleukin-8, and beta-defensin-2 after stimulation with peptidoglycan. These results provide evidence for a novel function of corticosteroids in airway inflammatory disorders, and indicate that the use of inhaled corticosteroids in such disorders may have a beneficial role in host defense mechanisms.
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PMID:Corticosteroid and cytokines synergistically enhance toll-like receptor 2 expression in respiratory epithelial cells. 1524 47

Ghrelin, a novel growth hormone-releasing peptide, has been shown to cause a positive energy balance by reducing fat use and stimulating food intake. This study investigated whether plasma ghrelin is associated with clinical parameters in patients with chronic obstructive pulmonary disease. Plasma ghrelin was measured in 50 patients and 13 control subjects, together with anabolic and catabolic factors. Patients were divided into two groups based on body mass index: underweight patients (n = 26) or normal weight patients (n = 24). Plasma ghrelin was significantly higher in underweight patients than in normal weight patients and healthy control subjects. Circulating tumor necrosis factor-alpha, interleukin-6, and norepinephrine were significantly higher in underweight patients than in normal weight patients. Plasma ghrelin correlated negatively with body mass index and correlated positively with catabolic factors such as tumor necrosis factor-alpha and norepinephrine. In addition, plasma ghrelin correlated positively with percent predicted residual volume and residual volume-to-total lung capacity ratio. In conclusion, plasma ghrelin was elevated in underweight patients with chronic obstructive pulmonary disease, and the level was associated with a cachectic state and abnormality of pulmonary function.
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PMID:Elevated plasma ghrelin level in underweight patients with chronic obstructive pulmonary disease. 1527 96


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