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

Physiological levels of human fibrinogen markedly inhibited the chemotactic activity of human neutrophils triggered by zymosan-activated serum (ZAS), C5a, or IL-8 in a Boyden chamber assay. Fibrinogen also slightly inhibited the N-formyl-methionyl leucyl-phenylalanine (FMLP)-induced migration of human neutrophils. Albumin was devoid of the inhibitory activities displayed by fibrinogen in this system. The inhibition of chemotaxis by fibrinogen was dose-dependent and saturable. Fibrinogen placed in the upper compartment of the Boyden chamber produced a larger inhibition than that obtained with fibrinogen placed in the lower compartment. Lysine as well as the lysine analog 6-aminohexanoic acid (AHA) decreased the inhibitory capacity of fibrinogen. In contrast, both arginine and glutamine failed to suppress the fibrinogen-mediated inhibition of neutrophil chemotaxis. AHA counteracts the inhibition of ZAS-induced chemotaxis by anti-CD18 monoclonal antibody, suggesting that lysine binding sites are required for integrin function in chemotaxis. Fibrinogen also inhibited, in a dose-dependent manner, the oxygen consumption of neutrophils activated by opsonized zymosan. Taken together, the present results indicate that fibrinogen modulates neutrophil functions and suggest that in addition to its role in blood coagulation, circulating fibrinogen may be involved in regulation of the inflammatory response.
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PMID:Inhibition of neutrophil activation by fibrinogen. 784 97

Renal tubulointerstitial injury is characterized by inflammatory cell infiltrate; however, the stimuli for leukocyte recruitment are not fully understood. IL-8 is a potent chemokine produced by proximal tubular epithelial cells (PTECs). Whether nephrotic proteins stimulate tubular IL-8 expression remains unknown. Acute exposure of human PTECs to albumin induced IL-8 gene and protein expression time- and dose-dependently. Apical albumin predominantly stimulated basolateral IL-8 secretion. Electrophoretic mobility shift assay demonstrated nuclear translocation of NF-kappaB, and the p65/p50 subunits were activated. NF-kappaB activation and IL-8 secretion were attenuated by the NF-kappaB inhibitors pyrrolidine dithiocarbamate and cell-permeable peptide. Albumin upregulated intracellular reactive oxygen species (ROS) generation, while exogenous H2O2 stimulated NF-kappaB translocation and IL-8 secretion. Albumin-induced ROS generation, NF-kappaB activation, and IL-8 secretion were endocytosis- and PKC-dependent as these downstream events were abrogated by the PI3K inhibitors LY294002 and wortmannin, and the PKC inhibitors GF109203X and staurosporin, respectively. In vivo, IL-8 mRNA expression was localized by in situ hybridization to the proximal tubules in nephrotic kidney tissues. The intensity of IL-8 immunostaining was higher in nephrotic than non-nephrotic subjects. In conclusion, albumin is a strong stimulus for tubular IL-8 expression, which occurs via NF-kappaB-dependent pathways through PKC activation and ROS generation.
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PMID:Albumin stimulates interleukin-8 expression in proximal tubular epithelial cells in vitro and in vivo. 1258 90

The aim of this prospective study was to determine the local concentrations of inflammatory mediators in various tissue types frequently affected by trauma to estimate the role of prestored cytokine release by mechanical tissue trauma in the induction of a systemic inflammatory response syndrome. The degree of tissue damage, evaluated by its systemic release of inflammatory mediators, represents an important factor concerning the outcome of trauma patients. Clinical trials indicate that the kind of traumatized tissue influences the cytokine pattern measured in patients blood afterwards. However, the tissue-specific mediator composition underlying this systemic mediator release is rarely elucidated. Upon approval of the local IRB/EC, skin, subcutaneous fat, muscle, cancellous bone, and lung tissue were obtained during standard surgical procedures. The protein-based concentrations of Interleukin (IL)-6, IL-8, IL-10, and IL-12 were determined in tissue homogenates by enzyme-linked immunoabsorbant assay (ELISA; n = 60 samples). Albumin was measured to evaluate the degree of blood contamination of tissue samples. IL-6 and IL-8 were consistently detectable in more than 95% of the tissue specimens. Lung and cancellous bone presented by far the highest concentrations of these cytokines, whereas skin, subcutaneous fat, and muscle showed significantly lower levels. IL-10 was not detectable in 88%; IL-12 could not be measured in 63% of the samples. Cytokine concentrations did not correlate with the amount of albumin measured in tissue specimens. Due to their consistent presence at the tissue level, high systemic concentrations of IL-6 and IL-8 in patients blood, seen after pulmonary trauma, long bone fractures, or soft tissue injury, may be interpreted as an overspill of local trauma mediators. This indicates their relevance in post-traumatic monitoring. Furthermore, albumin is a suitable and necessary indicator to evaluate influences of possible blood contamination in tissue samples.
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PMID:The pattern of preformed cytokines in tissues frequently affected by blunt trauma. 1268 38

OBJECTIVE: The aims of this study were to evaluate inflammatory cells, the profile of inflammatory mediators in nasal lavage (NL), and the involvement of the paranasal mucosa in atopic infants with no symptoms of sinusitis. METHODS: 48 atopic patients with allergic rhinitis (AR), and 33/48 patients with asthma were studied; the control group consisted of 13 nonatopic children. Those individuals with acute, chronic or recurrent sinusitis were excluded. The involvement of the paranasal mucosa was assessed by coronal computed tomography (CT) and graded by a standard protocol (0-30). A CT score greater than or equal to 12 indicated extensive involvement. Nasal lavage was used to quantify total and differential nasal cell counts. An aliquot of the supernatant was used for determining inflammatory mediators: interleukin-8 (IL-8), myeloperoxidase (MPO), and eosinophil cationic protein (ECP). Albumin was used as a marker for increased vascular permeability. These measurements were performed on all of the atopic patients and in 6/13 patients in the control group. The three groups were submitted to spirometry and complete blood cell count. RESULTS: Extensive involvement of the paranasal mucosa was observed in 7/33 (21%) of asthmatic patients (Group I) and 2/15 (13%) of those with allergic rhinitis (Group II). The highest CT score in the control group (Group III) was 7. Total cell and eosinophil count/ml and albumin concentration in nasal fluid were higher in asthmatic patients whose CT score was greater than 12. Interleukin-8 concentration, number of neutrophils and epithelial cells/ml in nasal fluid were similar in the three groups. A positive correlation between CT score, peripheral blood eosinophilia, number of eosinophils/ml and eosinophil cationic protein concentration was found in the nasal fluid of atopic children (n=48). There was an association between number of neutrophils and titers of interleukin-8 and myeloperoxidase, and between interleukin-8 and eosinophil count. CONCLUSIONS: in asthmatic patients with no symptoms of sinusitis, the extensive involvement of the paranasal mucosa is associated with blood and nasal lavage eosinophilia and cellular activation. Neutrophil infiltration and activation were not related to increased involvement of the paranasal mucosa.
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PMID:[Inflammatory mediators, cell counts in nasal lavage and computed tomography of the paranasal sinuses in atopic children] 1464 58

Little is known about the involvement of saliva in gingival overgrowth (GO). It was hypothesized that, in this situation, the composition of saliva is altered. Thus, proteins, albumin, cytokines, and growth factors in whole and glandular saliva were investigated. Differences between glandular and gingival contributions to the composition of saliva were explored in patients medicated with cyclosporin who exhibited GO (responders), those without GO (non-responders), and non-medicated subjects (controls). In whole saliva, interleukin-1alpha (IL-1alpha), IL-6, IL-8, epidermal growth factor (EGF), nerve growth factor (NGF), and albumin were detected, but in glandular saliva only EGF and NGF were identified. Albumin and IL-6 differed significantly between responders and controls, although the overall profile of salivary proteins remained unchanged. Thus, inflammatory cytokines and albumin are confined to whole saliva and are associated with GO, whereas its content of EGF and NGF appears unaffected by cyclosporin.
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PMID:Salivary proteins and cytokines in drug-induced gingival overgrowth. 1504 7

Tick-borne encephalitis (TBE) is one of the most frequent arthropod-transmitted viral diseases in Europe. Different vaccines against TBE-virus have been developed; a thimerosal-free and also albumin-free vaccine [Ticovac (Baxter Hyland Immuno, Vienna)] was approved in 2000. Contrary to previous experience, 779 cases of fever occurred following the first vaccination of children under 15 years of age and in 62 children febrile convulsions were even observed. Consequently, the composition of the vaccine was changed and albumin was again added [FSME-Immun (Baxter Vaccines, Vienna)] in 2001. The new Encepur Kinder (Chiron-Behring, Marburg) from 2002 is a TBE-vaccine for children without any protein as stabilizer but with a relatively high concentration of sucrose, while the former vaccine Encepur K from 1991 contained polygeline as the stabilizer. The induction of the immune system by the different TBE virus vaccines was compared in an in vitro test in order to find an explanation for the unexpected fever attacks. Whole blood was stimulated with complete vaccine suspension, and TNF-alpha, IL-1beta, IL-6, and IL-8 were determined from heparin/EDTA-plasma and culture supernatants. It was shown that Ticovac and the new Encepur Kinder can induce relatively high amounts of TNF-alpha and lower amounts of IL-1beta. An increase of both cytokines was first observed following an incubation of 4 hours, with a maximum after 15 hours. Concentrations returned to base-line values within 26 hours. The behaviour of both cytokines correlates with the febrile phases in children up to two years old. Albumin or other proteins like polygeline and also immunoglobulins prevented a rise of cytokines.
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PMID:Stimulation of the immune system by different TBE-virus vaccines. 1514 96

Exhaled markers of airway inflammation become increasingly important in the management of childhood asthma. The aims of the present study are: 1) to compare exhaled markers of inflammation (nitric oxide, carbon monoxide, and acidity of breath condensate) with conventional asthma measures (lung function tests and asthma control score) in childhood asthma; and 2) to investigate the detectability of albumin, CRP, IL-6, IL-8, TNF-alpha, sICAM-1, and sTNF-R75 in the exhaled breath condensate (EBC) of asthmatic children. Thirty-two children with mild to moderate persistent asthma and healthy controls aged 6-12 years were studied. We measured exhaled NO and CO, and subsequently EBC was collected. Inflammatory mediators in EBC were measured using an enzyme-linked immunosorbent assay. Respiratory symptoms and asthma control were assessed using the asthma control questionnaire (ACQ) of Juniper et al. (Eur Respir J 1999;14:902-907). Exhaled NO showed a significant correlation with exhaled CO (r = 0.59, P < 0.05) and FEV1 (r = -0.59, P < 0.05), but not with ACQ score (r = 0.48, P = 0.06). Exhaled CO was correlated with prebronchodilator FEV1 (r = -0.45, P < 0.05), but not with asthma control (r = 0.18, P = 0.35). Acidity of EBC was significantly lower in asthmatic children than in healthy controls (P < 0.05), but did not correlate with any of the conventional asthma measures. We were not able to demonstrate the presence of CRP, IL-6, IL-8, TNF-alpha, sICAM-1, and sTNF-R75 in EBC. Albumin was found in two EBC samples of asthmatic children. We conclude that exhaled NO had a better correlation with lung function parameters and asthma control than exhaled CO and acidity of EBC, in mild to moderate persistent childhood asthma. However, exhaled NO, CO, and deaerated pH of EBC did not differ between asthmatic children and controls, possibly because of a too homogeneous and well-controlled study population. To further evaluate the clinical utility of exhaled markers in monitoring childhood asthma, more studies are required on a wider range of asthma severity, and preferably with repeated measurements of markers and of asthma control.
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PMID:Childhood asthma: exhaled markers of airway inflammation, asthma control score, and lung function tests. 1521 92

We have recently shown that albumin added to meconium before intratracheal instillation in newborn pigs limits detrimental effect on the lungs and reduces increase of IL-8. The aim of this study was to test the effect of albumin instillation as rescue treatment in meconium aspiration syndrome (MAS). MAS was induced in hypoxic piglets by lung instillation of meconium (MAS I = 675 mg/kg, n=12; MAS II=540 mg/kg, n=14). Morbidity and mortality differed (MAS I, dead=7/12; MAS II, dead=5/14). MAS groups were randomized to postmeconium instillation of either bovine albumin (30%, 1.4 mL/kg; MAS I, n=6; MAS II, n=7) or isotonic saline (9 mg/mL, 1.4 mL/kg; MAS I, n=6; MAS II, n=7). The controls (n=4) were tested by sequential instillation of saline (9 mg/mL, 5 mL/kg) and albumin (30%, 1.4 mL/kg). Lung function and gas exchange deteriorated significantly after instillation of meconium [oxygenation index (OI): MAS I, +814%; MAS II, +386%; ventilation index (VI): MAS I, +256%; MAS II, +162%; compliance: MAS I, -53%; MAS II, -44%]. Increases of tracheal IL-8 correlated to deterioration of lung function were 10- (MAS I) and 5-fold (MAS II) (p <0.001). Lung compliance was higher in albumin instillation versus saline instillation (MAS I, p=0.008; MAS II, p=0.002). Albumin did not influence intergroup differences in IL-8, hemodynamics, OI, or VI. MAS-induced IL-8 increases correlated with deterioration of lung function (OI, VI, and compliance). Rescue treatment with albumin in meconium aspiration improved lung compliance in piglets and may represent a new therapeutic approach to MAS.
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PMID:Meconium induced IL-8 production and intratracheal albumin alleviated lung injury in newborn pigs. 1563 49

NF-kappaB is an ideal target for inhibition of proinflammatory cytokines. The purpose of this study was to determine if microencapsulated antisense oligomer to NF-kappaB can inhibit proinflammatory cytokine release in response to Escherichia coli endotoxin and bacteria. Microencapsulation takes advantage of the phagocytic function of the macrophage to deliver the oligomer intracellularly and enhance the effect. Albumin microcapsules 1 microm in size were prepared by a nebulization method containing antisense oligomers to NF-kappaB. E. coli endotoxin was incubated in 1 ml aliquots of whole blood. Microencapsulated antisense to NF-kappaB was given, and the inhibition of tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-6, and IL-8 was compared with similar amounts of oligomer in solution. Endotoxic shock was produced in rats using E. coli endotoxin (15 mg/kg). Peritonitis was induced by injecting 10(10) CFU E. coli. Cytokines were measured after simultaneous and delayed (4 h) administration of antisense to NF-kappaB in microcapsules and solution form. TNF was suppressed by 81% in whole blood, 56% in the endotoxic shock model, 89% in the peritonitis model (simultaneous treatment), and 56% in the delayed treatment group. Survival was 70% in the endotoxic shock group, 80% in the simultaneous peritonitis group, and 70% in the delayed treatment group. Microcapsule treatment using antisense to NF-kappaB suppressed TNF and IL-1 levels and mortality significantly better than all solution treatment groups in the whole blood model, endotoxic shock model, and peritonitis model.
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PMID:Treatment of experimental septic shock with microencapsulated antisense oligomers to NF-kappaB. 1595 54

The oxidation theory proposes that LDL oxidation is an early event in atherosclerosis and that oxidized LDL contributes to atherogenesis in triggering inflammation. In contrast to the copper-modified LDL, there are few studies using myeloperoxidase-modified LDL (Mox-LDL) as an inflammation inducer. Our aim is to test whether Mox-LDL could constitute a specific inducer of the inflammatory response. Albumin, which is the most abundant protein in plasma and which is present to an identical concentration of LDL in the intima, was used for comparison. The secretion of IL-8 by endothelial cells (Ea.hy926) and TNF-alpha by monocytes (THP-1) was measured in the cell medium after exposure of these cells to native LDL, native albumin, Mox-LDL, or Mox-albumin. We observed that Mox-LDL induced a 1.5- and 2-fold increase (ANOVA; P < 0.001) in IL-8 production at 100 microg/mL and 200 microg/mL, respectively. The incubation of THP-1 cells with Mox-LDL (100 microg/mL) increased the production of TNF-alpha 2-fold over the control. Native LDL, albumin, and Mox-albumin showed no effect in either cellular types. The myeloperoxidase-modified LDL increase in cytokine release by endothelial and monocyte cells and by firing both local and systemic inflammation could induce atherogenesis and its development.
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PMID:Triggering of inflammatory response by myeloperoxidase-oxidized LDL. 1716 45


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