Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis can to a certain extent be regarded as an inflammatory disease. Also, inflammatory markers may provide information about cardiovascular risk. Whether macrolide antibiotics, especially clarithromycin, have an anti-inflammatory effect in patients with atherosclerosis is not exactly known. To study this phenomenon, a placebo-controlled, randomized, double-blind study was performed. A total of 231 patients with documented coronary artery disease received a daily dose of either 500 mg of slow-release clarithromycin or placebo until the day of surgery. Levels of inflammatory markers (C-reactive protein, interleukin-2 receptor [IL-2R], IL-6, IL-8, and tumor necrosis factor alpha) were assessed during the preoperative outpatient visit, on the day of surgery, and 8 weeks after surgery. Also, changes in the levels of inflammatory markers between visits were determined by delta calculations. Baseline patient characteristics were balanced between the two treatment groups: the average age was 66 years (standard deviation [SD] = 9.0), 79% of the patients were male, and the average number of tablets used was 16 (SD = 9.3). The inflammatory markers of the groups as well as the delta calculations were not significantly changed. Treatment with clarithromycin did not influence the inflammatory markers in patients with atherosclerosis.
 ...
PMID:Effect of clarithromycin on inflammatory markers in patients with atherosclerosis. 1285 80

Long-term risk of mortality in patients with myocardial infarction is thought to be linked with plasma concentrations of proinflammatory cytokines and CRP (markers of inflammation). The aim of our study was to analyze plasma levels of interleukin (IL) 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction. One hundred and seven (107) patients with myocardial infarction hospitalized at the Cardiac Care Unit of St. Elizabeth's Sisters' Hospital in Warsaw and a control group of 10 subjects were enrolled in our study. The samples of peripheral venous blood were withdrawn from the patients on 2nd and 7th of infarction and plasma levels of IL-1, IL-6, IL-8 and CRP were determined. The patients were followed-up for a year. The analysis of survivals and deaths caused by acute coronary syndrome allowed to determine the predictive value of IL-1, IL-6, IL-8 and CRP in myocardial infarction. Twenty-two (22) of the total 107 patients died of acute coronary syndrome during one-year follow-up. Plasma IL-6 and CRP levels were higher in non-survivors as compared to the levels of IL-6 and CRP in living subjects, whereas plasma levels of IL-1 and IL-8 were comparable in both groups. IL-6 and CRP proved to be of predictive value in patients with myocardial infarction during one-year follow-up. It has also been found that plasma IL-6 level correlates with plasma CRP concentration and that there is a positive correlation between the former and CK-MB levels. IL-6 and CRP levels were higher in patients with Q wave infarction in comparison with non-Q wave infarction. Plasma levels of IL-1 and IL-8 have not been found to be good predictors of death during 12-month follow-up.
 ...
PMID:[Predictive value of plasma interleukin 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction]. 1287 62

Large-scale trials established that statin administration in hypercholesterolaemic individuals and patients with coronary heart disease (CHD) significantly reduces the risk of vascular events and death. This benefit was primarily attributed to their actions on lipids. This review focuses on the benefits (clinical and experimental) of statins observed soon (approximately 12 weeks) after their administration. Statins rapidly increase nitric oxide production and improve endothelial function (e.g. increased flow-mediated dilatation). Similarly, antioxidant properties decrease the susceptibility of low density lipoprotein cholesterol to oxidation. Statins inhibit the migration of macrophages and smooth muscle cell proliferation leading to an antiproliferative effect and the stabilisation of atherosclerotic plaques. Anti-inflammatory effects include a reduction in serum C-reactive protein levels, inflammatory and proinflammatory cytokines (e.g. IL-6, IL-8), adhesion molecules (e.g. ICAM-1, VCAM-1) and other acute phase proteins. Statins influence the haemostatic system. They reduce tissue factor expression and platelet activity, whereas fibrinolysis can be enhanced. Statins improve microalbuminuria, renal function, hypertension and arterial wall stiffness. A significant reduction of the carotid intima media thickness (IMT) was also reported early after statin treatment. These early effects of statins probably contribute to the significant reduction in vascular events seen in some 'short-term' studies. There is a need to further elucidate the rapid and non-lipid lowering properties of statins.
 ...
PMID:Early vascular benefits of statin therapy. 1459 27

Free radical-mediated changes in vascular permeability and subsequent inflammatory response may be a contributory pathogenetic cofactor responsible for the development of neurological sequelae associated with acute mountain sickness (AMS). To investigate this, 49 subjects were examined at sea level and serially after rapid ascent to 4,559 m. Although the venous concentration of total creatine phosphokinase activity was measured in all subjects, a complementary examination of lipid peroxidation (F(2)-isoprostanes), inflammatory (TNF-alpha, IL-1beta, IL-2, IL-6, IL-8, C-reactive protein), and cerebrovascular tissue damage (neuron-specific enolase) biomarkers was confined to a subcohort of 24 subjects. A selective increase (P < 0.05) in total creatine phosphokinase was observed in subjects diagnosed with AMS at high altitude (n = 25) compared with apparently healthy controls (n = 24). However, despite a marked increase in IL-6 and C-reactive protein attributable primarily to subjects developing high-altitude pulmonary edema, subcohort analyses demonstrated no selective differences in F(2)-isoprostanes, neuron-specific enolase, or remaining proinflammatory cytokines due to AMS (n = 14). The present findings are the first to demonstrate that free radical-mediated neuronal damage of sufficient degree to be detected in the peripheral circulation does not occur and is, therefore, unlikely to be an important, initiating event that is critical for the development of AMS. The pathophysiological significance of increased sarcolemmal membrane permeability and inflammatory response, either as a cause or epiphenomenon of AMS and/or high-altitude pulmonary edema, remains to be elucidated.
 ...
PMID:Pathophysiological significance of peroxidative stress, neuronal damage, and membrane permeability in acute mountain sickness. 1459 61

The purpose of this study was to semiquantify the magnitude of surgical stress in patients undergoing aortic surgery by measuring inflammatory responses perioperatively, focusing on cytokine secretion. Serum concentrations of interleukin (IL) 1alpha, IL-6, IL-8, and tumor necrotizing factor (TNF) Alpha were measured in patients undergoing abdominal or thoracic aortic aneurysmectomy preoperatively and periodically thereafter for 2 weeks. Urinary trypsin inhibitor (UTI/Cr) and C-reactive protein (CRP) concentration and the systemic inflammatory response syndrome (SIRS) score also were determined. Indices of inflammation and cytokine concentrations peaked at 1-3 days after surgery and decreased thereafter; however, IL-8 increased again after day 7. Concentrations of IL-8, UTI/Cr, and CRP and the SIRS score were still higher 14 days after surgery than preoperatively. The maximum concentrations of IL-6 and IL-8 were higher after thoracic than abdominal aortic repair; however, the maximum values of cytokines were not correlated with operative factors in all patients. A patient suffering from graft infection showed an increase in cytokine concentrations on day 7. The inflammatory response does not return to preoperative values within 2 weeks of surgery in patients undergoing thoracic or abdominal aortic aneurysm repair. The prolonged secretion of IL-8 suggests a host reaction to the synthetic prosthesis. A large increase in inflammatory cytokines on day 7 may indicate infection of the vascular graft.
 ...
PMID:Vascular prosthetic implantation is associated with prolonged inflammation following aortic aneurysm surgery. 1459

The evolution and the relationship between inflammatory and renal-injury markers in women with acute uncomplicated pyelonephritis under antimicrobial therapy were investigated in a prospective study. Markers were measured before and 6 and 24 h after the intravenous administration of 1 g of ceftriaxone. Before treatment, the median levels of all markers except the serum creatinine levels were high. Twenty-four hours after the onset of antibiotic treatment, the C-reactive protein (CRP) level continued to be high, while the serum interleukin-6 (IL-6) levels and the urine IL-6, IL-8, albumin, and immunoglobulin G (IgG) levels decreased significantly. In contrast, serum creatinine and tumor necrosis factor alpha levels and urine N-acetyl-beta-glucosaminidase, alpha1-microglobulin, and beta2-microglobulin levels did not change over time. There was a significant correlation between IL-6 and IL-8 levels and urine albumin and IgG levels (urine albumin and IgG levels are glomerular and urinary tract-injury markers) as well as between serum CRP levels and the levels of the tubular-injury markers. In women with acute pyelonephritis, appropriate antibiotic treatment rapidly decreases serum IL-6 levels and urine IL-6 and IL-8 levels, which correlate well with urine albumin and IgG levels.
 ...
PMID:Evaluation of inflammatory and renal-injury markers in women treated with antibiotics for acute pyelonephritis caused by Escherichia coli. 1471 61

Inflammation plays a pivotal role in atherosclerosis. In addition to being a risk marker for cardiovascular disease, much recent data support a role for C-reactive protein (CRP) in atherogenesis. Interleukin-8 (IL-8), a member of the CXC chemokines promotes monocyte-endothelial cell adhesion and arrest and is abundant in atherosclerotic plaques. However, there is a paucity of data examining the effect of CRP on IL-8 secretion in human aortic endothelial cells (HAEC). In this report, we show that incubation of HAEC with CRP resulted in a time and dose-dependent increase in IL-8 protein and mRNA via transcription. In contrast to human umbilical vein endothelial cells, monocyte-chemoattractant protein-1 expression in HAEC was not affected by CRP. Furthermore, CRP upregulated NF-kappa B activity in HAEC and inhibitors of NF-kappa B significantly reversed the upregulation of IL-8 by CRP. Blocking antibodies to IL-8 significantly decreased monocyte-endothelial cell adhesion induced by CRP (31%, P<0.01). In conclusion, this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity.
 ...
PMID:Effect of C-reactive protein on chemokine expression in human aortic endothelial cells. 1501 Feb 79

The brain tissue damage after stroke is mediated partly by inflammation induced by ischaemia-reperfusion injury where the complement system plays a pivotal role. In the present study we investigated systemic complement activation and its relation to C-reactive protein (CRP), a known complement activator, and other inflammatory mediators after acute ischaemic stroke. Sequential plasma samples from 11 acute stroke patients were obtained from the time of admittance to hospital and for a follow-up period of 12 months. Nine healthy gender- and age-matched subjects served as controls. The terminal SC5b-9 complement complex (TCC), CRP, soluble adhesion molecules (L-, E- and P- selectin, ICAM, VCAM) and cytokines [tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-8] were analysed. All parameters were within normal values and similar to the controls the first hours after stroke. Terminal complement complex (TCC) increased significantly from 0.54 to 0.74 AU/ml at 72 h (P = 0.032), reached maximum at 7 days (0.90 AU/ml, P < 0.001), was still significantly increased at 12 days (0.70 AU/ml, P = 0.009) and thereafter normalized. CRP increased significantly from 1.02 to 2.11 mg/l at 24 h (P = 0.023), remained significantly increased for 1 week (2.53-2.94 mg/l, P = 0.012-0.017) and thereafter normalized. TCC and C-reactive protein (CRP) correlated significantly (r = 0.36, P < 0.001). The increase in TCC and CRP correlated to the size of infarction (r = 0.80 and P = 0.017 for TCC; r = 0.72 and P = 0.043 for CRP). No significant changes were seen for adhesion molecules and cytokines. In conclusion, transitory systemic complement activation takes place after stroke. The early rise in CRP and the following TCC increase suggest a possible role for CRP in complement activation, which may contribute to inflammation after stroke.
 ...
PMID:Systemic complement activation following human acute ischaemic stroke. 1519 51

Acute and chronic hyperglycemia are proinflammatory states, but the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks is not known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH). We studied 20 lean and 28 obese patients with DKA, 10 patients with NKH, and 12 lean and 12 obese nondiabetic control subjects. We measured 1) proinflammatory cytokines (tumor necrosis factor-alpha, interleukin [IL]-6, IL1-beta, and IL-8), 2) markers of cardiovascular risk (C-reactive protein [CRP], homocysteine, and plasminogen activator inhibitor-1 [PAI-1]), 3) products of reactive oxygen species (ROS; thiobarbituric acid [TBA]-reacting material, and dichlorofluorescein [DCF]), and 4) cortisol, growth hormone (GH), and free fatty acids (FFAs) on admission (before insulin therapy) and after insulin therapy and resolution of hyperglycemia and/or ketoacidosis. Results were compared with lean and obese control subjects. Circulating levels of cytokines, TBA, DCF, PAI-1, FFAs, cortisol, and GH on admission were significantly increased two- to fourfold in patients with hyperglycemic crises compared with control subjects, and they returned to normal levels after insulin treatment and resolution of hyperglycemic crises. Changes in CRP and homocysteine in response to insulin therapy did not reach control levels after resolution of hyperglycemia. We conclude that DKA and NKH are associated with elevation of proinflammatory cytokines, ROS, and cardiovascular risk factors in the absence of obvious infection or cardiovascular pathology. Return of these values to normal levels with insulin therapy demonstrates a robust anti-inflammatory effect of insulin.
 ...
PMID:Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. 1527 89

The possible association between mediators of inflammation such as cytokines and perinatal colonization of the respiratory tract remains unclear. This prospective cohort study evaluated endotracheal colonization in 141 ventilated preterm infants at birth. The relation with cytokine response in the airways and C-reactive protein (CRP) in umbilical blood was investigated. Of the 141 preterm infants enrolled in this study, 37 (26%) were colonized. In addition to traditional pathogens (61%), commensal species (26%) and Mycoplasmataceae (13%) were isolated. Both the pro-inflammatory cytokines IL-1 beta, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha as well as the antiinflammatory IL-10 are increased in colonized patients in a dose-dependent manner, with the strongest response in neonates colonized with Gram-negative organisms. There was no antimicrobial IL-12p70 response in colonized infants. Commensal flora is associated with the same inflammatory response as traditional pathogens. Although the umbilical cord blood CRP level was significantly higher in neonates with endotracheal colonization, it was highest in those colonized with Gram-negative organisms but still close to normal limits. Microorganisms in the endotracheal fluid of ventilated preterm infants are associated with a pathogen-specific and dose-dependent cytokine response in the airways and systemic CRP response.
 ...
PMID:Endotracheal colonization at birth is associated with a pathogen-dependent pro- and antiinflammatory cytokine response in ventilated preterm infants: a prospective cohort study. 1529 95


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>