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)

We studied longitudinally inflammatory reactions and serum C-reactive protein (S-CRP) levels in 52 colorectal cancer patients treated with a median of six 3-weekly cycles of raltitrexed 1.5-3.0 mg m(-2) combined with oral carmofur (1-hexylcarbomoyl-5-fluorouracil) 300-400 mg m(-2) on cycle days 2-14. Thirty-nine (75%) of these patients had fever on days 2 to 9 after receiving raltitrexed, 49 (94%) had fatigue Gr. > or = 1, and 49 (94%) elevated S-CRP without a documented infection. The systemic inflammatory composite score (consists of body temperature, fatigue, S-CRP, interleukin-6 (S-IL-6), S-IL-8, and tumour necrosis factor-alpha (S-TNF alpha) levels) was calculated in a cross-sectional one-cycle study involving 60 colorectal cancer patients treated with single-agent raltitrexed, raltitrexed and carmofur, or 5-fluorouracil-based chemotherapy (n=20 in each group). The median S-CRP, S-IL-6, and S-TNF alpha levels were higher 7 days after giving raltitrexed (57 vs 23 mg l(-1), 64 vs 10 ng l(-1), and 11 vs 10 ng l(-1), respectively) or raltitrexed+carmofur (142 vs 10 mg l(-1), 64 vs 10 ng l(-1), and 16 vs 9 ng l(-1), respectively) than at baseline (P<0.01 for each comparison), but not when 5-fluorouracil-based regimens were administered. These findings suggest that colorectal cancer patients treated with raltitrexed may develop drug-related systemic inflammation, which may be difficult to discriminate from infection.
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PMID:Raltitrexed treatment promotes systemic inflammatory reaction in patients with colorectal carcinoma. 1223 67

Hormone replacement therapy (HRT) reduces the risk for osteoporosis but transiently increases cardiovascular risk for some postmenopausal women. This study investigated the hypothesis that these risks are associated with HRT-induced changes in mononuclear cell secretion of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and associated soluble receptors. Compared to the untreated condition (n=8), estrogen therapy (n=7) and estrogen+progestin therapy (n=7) both caused 2-fold elevations in TNF-alpha secretion. IL-6 secretion was increased (48%, P=0.04) only by estrogen+progestin therapy. Although soluble receptor secretion was not different among groups, soluble TNF receptor type I and IL-6 receptor secretion were inversely related to plasma follicle stimulating hormone (P<0.05). Both therapies reduced plasma osteocalcin (a marker for osteoporosis) by approximately 50% (P<0.002). Plasma C-reactive protein (CRP, a marker for cardiovascular risk) was 3-fold higher in women receiving only estrogen, compared to untreated women (P=0.01), and twice as high as those receiving estrogen+ progestin (P=0.045). Simple linear relationships were not observed between cytokine secretion and these markers, but a significant HRT/TNF-alpha interaction with osteocalcin (P=0.022) and an HRT/IL-6 interaction with CRP (P =0.016) indicated more complex relationships between hormone replacement, cytokine activity, and health risks associated with menopause.
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PMID:Hormonal modulation of interleukin-6, tumor necrosis factor and associated receptor secretion in postmenopausal women. 1229 13

Low plasma levels of the anti-inflammatory factor adiponectin characterize obesity and insulin resistance. To elucidate the relationship between plasma levels of adiponectin, adiponectin gene expression in adipose tissue, and markers of inflammation, we obtained blood samples, anthropometric measures, and subcutaneous adipose tissue samples from 65 postmenopausal healthy women. Adiponectin plasma levels and adipose-tissue gene expression were significantly lower in obese subjects and inversely correlated with obesity-associated variables, including high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6). Despite adjustment for obesity-associated variables, plasma levels of adiponectin were significantly correlated to adiponectin gene expression (partial r = 0.38, P < 0.05). Furthermore, the inverse correlation between plasma levels of hs-CRP and plasma adiponectin remained significant despite correction for obesity-associated variables (partial r = -0.32, P < 0.05), whereas the inverse correlation between adiponectin plasma levels or adiponectin gene expression in adipose tissue with plasma IL-6 were largely dependent on the clustering of obesity-associated variables. In conclusion, our data suggest a transcriptional mechanism leading to decreased adiponectin plasma levels in obese women and demonstrate that low levels of adiponectin are associated with higher levels of hs-CRP and IL-6, two inflammatory mediators and markers of increased cardiovascular risk.
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PMID:Association between adiponectin and mediators of inflammation in obese women. 1266 65

Hepatocyte growth factor (HGF) has been shown to be involved in angiogenesis, epithelial cell proliferation, and osteoclast activation. HGF and its receptor are expressed on myeloma cell lines and could be involved in the pathogenesis of bone destruction in multiple myeloma (MM). The aim of this study was to examine serum levels of HGF in untreated MM patients and its correlation with bone turnover indices and markers of disease activity. Forty-seven newly diagnosed MM patients and 25 controls were included: 12 patients were of stage I, 13 of stage II, and 22 of stage III (Durie-Salmon classification). Bone lesions were scored from 0 to 3, according to X-ray findings. Serum osteocalcin (OC), interleukin-6 (IL-6), TNF-alpha, beta(2)-microglobulin (beta(2)M), CRP, calcium, and 24-hr urine N-telopeptide cross-links of collagen breakdown (NTx) were determined. HGF levels were significantly higher at stage III compared to stages II and I (medians: 1,990.4 vs. 1,743.8 and 1,432.4 pg/mL, respectively, P < 0.05). Similarly, NTx, IL-6, TNF-alpha, CRP, beta(2)M, and calcium increased significantly with advancing stage (P < 0.01). OC was higher at stage I in comparison to stages II and III (P < 0.01). All parameters were significantly higher in patients than controls. HGF showed a strong correlation with IL-6 and TNF-alpha and less with beta(2)M, CRP, NTx, and OC. We conclude that serum HGF levels are increased in advanced stages of MM disease and extended bone lesions. HGF correlates with IL-6 and TNF-alpha, which are cytokines involved in osteoclast stimulation in MM. However, an independent association of HGF with bone turnover markers was not shown in this study, thus its role in MM bone disease needs to be further clarified.
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PMID:Elevated serum concentration of hepatocyte growth factor in patients with multiple myeloma: correlation with markers of disease activity. 1266 32

Echocardiography was routinely used in evaluating patients with cardiac myxoma, reflecting the improved capability of this technique to assess morphological findings. Recent studies reported that the immunologic findings, such as CRP(C-reactive protein) and IL-6(interleukin-6), were related to the clinical features in patients with cardiac myxoma. Therefore, the purpose of this study was to clarify whether the morphological findings were related to the immunologic and pathologic results in patients with cardiac myxoma. We studied 6 patients (2 men; mean age +/- SD, 62.5 +/- 10.4 years) with cardiac myxoma. Transthoracic and transesophageal echocardiography were used to assess morphological findings. All patients had not symptoms associated with obstruction of the intracardiac blood flow. Five of these 6 patients with increased levels of IL-6 had clinical features. In conclusion, assessment of morphological findings by echocardiography has the potential to infer the immunologic and pathologic results in patients with cardiac myxoma.
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PMID:[Comparison of echocardiographic and morphological findings in patients with left atrial myxoma]. 1270 2

Cigarette smokers frequently fail multiple attempts to quit smoking, often because of the unpleasant symptoms that accompany quitting. Similar unpleasant symptoms accompany inflammatory responses during infection and autoimmune disease. The hypothesis that smoking abstinence induces inflammation was tested. Eighteen smokers (n = 18) were evaluated while smoking freely and after 24 h of nicotine abstinence. Immune, cardiovascular and psychological measures were collected. Hunger, nervousness, anxiety, restlessness and irritability increased during abstinence (p < 0.05); systolic blood pressure and heart rate levels decreased (p < 0.05). Analysis demonstrated a split among smokers in response to abstinence compared with smoking freely; some smokers (n = 10) displayed increased C-reactive protein (CRP, p < 0.05) whereas others (n = 8) responded with decreased CRP (p < 0.05). An increase in symptoms of depressed mood and a fall in heart rate occurred only in those who displayed increased CRP with nicotine abstinence ( p < 0.05), while systolic blood pressure fell only in those whose CRP levels decreased with abstinence ( p < 0.05). Interleukin-1 and interleukin-6 did not change with abstinence. The results suggest that 24 h nicotine abstinence does not stimulate inflammation among all smokers, but that a sub-group of smokers do demonstrate an inflammatory response with significant negative psychological and physiological symptomatology.
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PMID:C-reactive protein and depressed mood in a sub-group of smokers during nicotine abstinence. 1285 18

Hypercholesterolemia causes endothelial dysfunction, an early feature of atherosclerosis, leading to increased production of adhesion molecules and cytokines. The aim of this study was to investigate the effects of three months of treatment with low dose atorvastatin on serum levels of adhesion molecules, interleukin-6 (IL-6) and highly sensitive C-reactive protein (hs-CRP) in patients with non-familial hypercholesterolemia. Fifty-five patients with non-familial hypercholesterolemia were randomized to treatment with atorvastatin 10 mg/day or placebo for 3 months. Soluble intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, IL-6 and hs-CRP levels were measured to assess the inflammatory activity of the endothelium. There was a significant reduction in ICAM-1 at 2 weeks (p<0.0001) with further reduction at 3 months (p<0.0001). At 3 months, there were significant reductions in VCAM-1 (p<0.02), IL-6 (p<0.0001) and hs-CRP (p<0.01), but an increase in E-selectin levels (p<0.002). Treatment with statin was an independent determinant of change in ICAM-1 (p<0.05) and IL-6 levels (p<0.05) after correcting for anthropometric indices, blood pressure and lipid profile. Low-dose atorvastatin treatment leads to reduction in proinflammatory markers of endothelial function, suggesting an attenuation of endothelial activation and improvement in endothelial function, independent of lipid lowering. This may lead to a reduction in the progression of atherosclerosis.
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PMID:Reduction in serum levels of adhesion molecules, interleukin-6 and C-reactive protein following short-term low-dose atorvastatin treatment in patients with non-familial hypercholesterolemia. 1295 65

Recent evidence associates inflammatory mediators with coronary heart disease. Elevation of acute-phase reaction (APR) proteins such as serum amyloid A, fibrinogen, CRP and haptoglobin in response to Helicobacter pylori (H. pylori) infection was shown to initiate gastritis and ischemic heart disease. Positive Chlamydia pneumoniae (C. pneumoniae) serology is associated with increased levels of inflammatory cytokines and tumor necrosis factor-alpha (TNF-alpha), which stimulates endothelial cell activation, procoagulant activity and angiogenesis in patients with coronary heart disease. As a final example, interleukin-6 (IL-6) has been proposed to mediate cardiovascular disorders. Public awareness of risks of excessive body weight and high levels of serum cholesterol propelled the development of synthetic dietary components such as sucrose polyester (SPE) to substitute for natural lipids. SPE is a synthetic lipid whose physical properties are similar to a natural triacylglycerol with a similar assortment of fatty acids and is resistant to lipolysis by gastric and pancreatic enzymes. Intake of SPE in lieu of natural lipids is expected to decrease absorption of essential fatty acids (EFA) and fat-soluble vitamins among other essentials. Deficiency of EFA leads to the formation of faulty cellular membranes, which is manifested as skin lesions, growth failure, erythrocyte fragility, impairment of fertility and uncoupling of oxidation and phosphorylation. Possibilities of absorption of these synthetic lipids into the circulation may represent an unexpected health hazard. We have shown that subcutaneous (sc) administration to rabbits of a range of lipolysis-resistant lipid-like sorbitol, mannitol and arabitol esters of palmitic (P) and lauric (L) acids was found to evoke a mild APR, which in humans could contribute to CHD incidence. We suggest a reversal in the commonly accepted role of SPE as a sequestor of dietary lipid: SPE may be the lipophilic solute contained within the dietary lipid solvent micelle. An alternative conclusion regarding the biological effects of excessive dose of SPE in human and pig for a short time span should be considered.
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PMID:Cardiac heart disease in the era of sucrose polyester, Helicobacter pylori and Chlamydia pneumoniae. 1496 37

Background: An association between Chlamydia pneumoniae (Cp) infection and coronary heart disease (CHD) has already been reported. We investigated the relationship between Cp infection and other risk factors in CHD patients, as well as the effects of azithromycin treatment. Methods: We studied 38 patients with Cp infection (Cp-pos) and 15 without (Cp-neg). Cp-pos patients had, both at inclusion and 2 years prior to inclusion, elevated Cp-specific IgA-antibodies, with or without the presence of pharyngeal Cp by polymerase chain reaction (PCR) detection. Blood was analyzed for Cp-antibodies, interleukin-6, interleukin-1 receptor antagonist (IL-1ra), CRP, orosomucoid, fibrinogen, leukocytes, PAI-1, tPA, von Willebrand factor (vWf), platelet count and aggregation, and lipids. Cp-pos patients were randomized to placebo or oral azithromycin, 500 mg on day 1 and then 250 mg/day for 4 days, with repeated therapy after 3 weeks. Blood was taken immediately, as well as 3 months and 2 years after therapy. Results: CRP and IL-1ra levels were higher in Cp-pos than in Cp-neg patients: median, interquartile range 8.5 (3.0-20) vs. 2.0 (1.0-3.8) mg/l, and 316 (165-404) vs. 178 (118-195) ng/l, p=0.0006 and p=0.002, and platelet aggregation was lower: 4.8 (2.9-6.4) vs. 8.1 (4.7-11.4) Omega, p<0.05. tPA levels increased in azithromycin-treated patients between entry and 3-month follow-up: mean+/-S.D. 3.7+/-4.2 vs. 1.0+/-2.1 microg/l, p<0.05. Other variables did not differ. Conclusions: Cp infection was associated with increased inflammatory activity and lower platelet aggregability, suggesting that inflammation may be of greater pathophysiological importance than platelet activity in these patients. Although an effect on Cp infection was not shown, azithromycin may have a positive effect on fibrinolysis, as increased levels of tPA were observed in the treatment group.
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PMID:Azithromycin therapy in patients with chronic Chlamydia pneumoniae infection and coronary heart disease: immediate and long-term effects on inflammation, coagulation, and lipid status in a double-blind, placebo-controlled study. 1496 98

Atherosclerosis is a chronic pathological process and it is generelly accepted that lipids, coagulation and inflammatory factors play an important role in its development. Environmental factors such as bed diet and cigarette smoking strongly stimulate initation and progression of atherosclerotic changes in the artery wall. It has been recognized that deeply processed food may be a source of various factors potentiating processes related to atherosclerosis development among which inflammatory processes are of great importance. The aim of our studies was to find out if the trans-unsaturated fatty acids as well as acrylamide present in foods have the potential to provoke pro-inflammatory states in the body and enhance atherosclerosis risk. The results of our in vitro studies have shown that trans fatty acids cause a significant increase in secretion of reactive oxygen species, interleukin-6, tumor necrosis factor a and metalloproteinase-9, and enhance apoptosis. It indicates that in vivo trans-fatty acids may distroy the endothelium integrity and cause plaque rupture. Our in vivo studies in the group of healthy volunteers have shown that the consumption of potato chips rich in acrylamide cause the significant increase in plasma C-reactive protein and homocysteine concentrations. Enhanced CRP and HCY levels are accepted markers of enhanced atherosclerosis risk.
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PMID:Trans-unsaturated fatty acids and acrylamide in food as potential atherosclerosis progression factors. Based on own studies. 1505 16


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