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)

The expression of cytokines that are potentially involved in the pathogenesis of vasculitis was studied in patients with primary systemic vasculitis (PSV). In extension of earlier reports, we detected an overexpression of transforming growth factor beta (TGF beta), interleukin 6 (IL6), and interleukin 8 (IL8), indicating that the whole cytokine cascade is activated to a significant extent in PSV.
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PMID:Pro- and anti-inflammatory cytokines in primary systemic vasculitis. 829 31

The plasma concentrations of type II phospholipase A2 (type II PLA2) and eicosanoids, such as leukotriene B4 (LTB4), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TXB2), were determined by radioimmunoassay in 23 patients with burns covering at least 20 per cent of their body surface. Cytokines such as tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and interleukin 8 (IL-8) were determined by enzyme-immunosorbent assay. There was no increase in type II PLA2 concentration in the early stage of burns, but an increase in type II PLA2 concentration was triggered by infection (P < 0.0001). The level of type II PLA2 was significantly higher in the non-surviving group than in the surviving group (P = 0.0006), suggesting that it reflects the severity of the disease. There was a significant correlation between the maximum level of type II PLA2 and TNF-alpha (r = 0.6346, P = 0.0011). There was a significant correlation between the maximum level of type II PLA2 and the accompanying plasma concentrations of LTB4, 6-keto-PGF1 alpha, and TXB2 throughout the observation period (r = 0.4814, P = 0.0200; r = 0.5943, P = 0.0028; r = 0.4368, P = 0.0372 respectively). Plasma levels of LTB4, and TXB2 were significantly higher in the burn patients who died than in those who survived (P = 0.0493; P = 0.0493 respectively).
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PMID:Plasma concentrations of type II phospholipase A2, cytokines and eicosanoids in patients with burns. 855 82

The presence and concentration of selected cytokines (interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 8 (IL-8), granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were evaluated in the sera of 12 burned patients (6-90 per cent body surface area). The presence of cytokines in the sera of 20 healthy volunteers (control group) was always undetectable (< 2 pg/ml). In sera of the burned patients the concentrations of IL-4 or GM-CSF were also below the test sensitivity levels, while G-CSF and IL-6 were present throughout all the observation period and IL-8 was detectable at the onset of massive infections. The serum concentrations of G-CSF and IL-6 increased during the episodes of clinically and bacteriologically detectable infections. Their increases were, however, observable 12-24 h later than the other infection symptoms. Similar increases in G-CSF and IL-6 levels have been detected during corrective surgery (covering of granulation tissue with skin grafts). It may be concluded that serum G-CSF and IL-6 levels in burned patients may be considered as diagnostic factors, but the delays in the reaction to the massive infection do not allow us to use them for predicting the time of onset of the infection.
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PMID:Serum cytokine levels (IL-4, IL-6, IL-8, G-CSF, GM-CSF) in burned patients. 855 85

Airway epithelial cells have a potential to participate in regulation of local homeostasis by releasing active compounds including cytokines and growth factors. Several factors such as transforming growth factor-beta and endothelin have been shown to regulate airway epithelial cell functions through an autocrine mechanism. We studied the expression of the specific receptor for a multifunctional cytokine interleukin 6 (IL-6), which is expressed and released by airway epithelial cells. Specific binding assay demonstrated a single set of binding sites on human primary and transformed bronchial epithelial cells. Human interleukin-1alpha (IL-1alpha) increased maximal binding sites to IL-6. Northern blot analysis demonstrated that airway epithelial cells constitutively expressed mRNA for IL-6 receptor (IL-6R), and IL-1alpha and IL-6 itself upregulated IL-6R gene expression. Moreover, exogenously added human recombinant IL-6 had a stimulatory effect on IL-8 release from human bronchial epithelial cells. These results indicated that human bronchial epithelial cells expressed IL-6R, and IL-6 might be involved in the regulation of the epithelial functions via an autocrine as well as a paracrine mechanism.
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PMID:Interleukin 6-receptor expression on human bronchial epithelial cells: regulation by IL-1 and IL-6. 863 26

Mammary epithelial cells (MECs) were isolated and cultured from mammary glands of healthy women undergoing reduction mammoplasty. Normal MECs were infected with the transforming hybrid virus adeno-5/SV40. Two transformed epithelial cell lines, M1 and M2, were obtained, characterised phenotypically and studied for the production of and the response to cytokines and growth regulators. In both cell lines, expression of the SV40 large T antigen was associated with loss of interleukin 6 (IL-6) production and responsiveness as well as with down-regulation of IL-8 and transforming growth factor (TGF)-alpha production. Both M1 and M2 cell lines were capable of forming colonies in semisolid media, but upon injection into severe combined immunodeficient (SCID) mice only M2 cells were tumorigenic. DNA synthesis in M1 cells was partially inhibited by serum or TNF-alpha and weakly stimulated by hydrocortisone (HC) and IL-8. In contrast, M2 cells were totally unresponsive to a variety of growth regulators. Both lines overexpressed the p53 protein at levels about 20-fold higher than those observed in primary MEC cultures, but no mutations of the p53 gene could be detected. The date confirm the view that the expression in human mammary cells of different oncogenes - including the SV40 T antigen - is frequently associated with alterations of cytokine production and responsiveness.
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PMID:Defective interleukin six expression and responsiveness in human mammary cells transformed by an adeno 5/SV40 hybrid virus. 864 79

We have developed a functional assay to study the inflammatory capacity of plasma collected from patients with severe gram-negative septic shock. In this assay, elutriation-purified, cryo-preserved human monocytes from one healthy donor are combined with plasma from patients with severe persistent septic shock for 5 h. Subsequently, the plasma is removed, medium added, and procoagulant activity (PCA) and secretion of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) measured after 18-h incubation. Plasma from 10 patients (6 died) infected with Neisseria meningitidis previously shown to contain high levels of native lipopolysaccharide (LPS) (median 2,700 pg/ml), TNF-alpha, IL-6, IL-8, and complement activation products, had a low net spontaneous inflammatory capacity on the monocytes. The median levels of PCA, TNF-alpha, and IL-6 were 5, 0, and 4%, respectively, of the monocyte activities induced by normal plasma boosted with purified N. meningitidis (Nm)-LPS (2,500 pg/ml; net LPS-boosted capacity, 100%). The levels of PCA, TNF-alpha, and IL-6 obtained with plasma from shock patients were not different from those induced by plasma from 10 meningococcal patients without shock or with plasma from healthy persons. Boosting shock plasma with 2,500 pg/ml Nm-LPS had little effect on the monocyte activities since the median values of PCA, TNF-alpha, and IL-6 revealed a minimal increase from 5, 0, and 4% to 9, 2, and 6%, respectively. The shock plasmas revealed a strong LPS-inhibitory capacity that was largely absent in plasmas from 10 meningococcal patients without shock since the median levels of PCA, TNF-alpha, and IL-6 increased from 5, 0, and 0% to 135, 51, and 73%, respectively, after boosting with 2,500 pg/ml Nm-LPS. The LPS-inhibitory capacity was closely associated with the levels of IL-10. The median levels of IL-10 were 19,000 pg/ml in nine shock patients vs. 22 pg/ml in nine nonshock patients with systemic meningococcal disease. Removal of native IL-10 by immunoprecipitation restored the capacity of plasmas to induce monocyte activation either by native LPS or by boosting with Nm-LPS. IL-4 and TGF-beta were not detected in shock plasmas. In 24 patients with detectable meningococcal LPS ( > 10 pg/ml, 0.1 endotoxin units/ml), the levels of IL-10 were correlated to the levels of LPS (r = 0.79, P < 0.001). IL-10 declined from initiation of antibiotic therapy and paralleled the levels of native LPS. Decreasing levels of IL-10 in serially collected shock plasmas were directly related to increasing monocyte responsiveness after Nm-LPS boosting. These results suggest that IL-10 plays a major role in containing activation of monocytes and possibly other LPS-responsive cells during overwhelming meningococcemia.
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PMID:Net inflammatory capacity of human septic shock plasma evaluated by a monocyte-based target cell assay: identification of interleukin-10 as a major functional deactivator of human monocytes. 869 Nov 49

Endothelial cells have the potential to influence significantly the host immune response to blood-borne microbial pathogens, such as Candida albicans. We investigated the ability (of this organism to stimulate endothelial cell responses relevant to host defense in vitro. Infection with C. albicans induced endothelial cells to express mRNAs encoding E-selectin, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, interleukin 6, interleukin 8, monocyte chemoattractant protein 1, and inducible cyclooxygenase (cox2). All three leukocyte adhesion molecule proteins were expressed on the surfaces of the endothelial cells after 8 h of exposure to C. albicans. An increase in secretion of all three cytokines was found after 12 h of infection. Cytochalasin D inhibited accumulation of the endothelial cell cytokine and leukocyte adhesion molecule mRNAs in response to C. albicans, suggesting that endothelial cell phagocytosis of the organism is required to induce this response. Live Candida tropicalis, Candida glabrata, a nongerminating strain of C. albicans, and killed C. albicans did not stimulate the expression of any of the cytokine or leukocyte adhesion molecule mRNAs. These findings indicate that a factor associated with live, germinating C. albicans is required for induction of endothelial cell mRNA expression. Furthermore, since endothelial cells phagocytize killed C. albicans, phagocytosis is likely necessary but not sufficient for this organism to stimulate mRNA accumulation. In conclusion, the secretion of proinflammatory cytokines and expression of leukocyte adhesion molecules by endothelial cells in response to C. albicans could enhance the host defense against this organism by contributing to the recruitment of activated leukocytes to sites of intravascular infection.
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PMID:Candida albicans stimulates cytokine production and leukocyte adhesion molecule expression by endothelial cells. 869 86

Plasma levels of type II phospholipase A2 (type II PLA2), cytokines and endotoxin were determined in patients with sepsis to investigate their interrelations and their role in the patient's prognosis. Type II PLA2 was measured by radioimmunoassay, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and IL-8 were each measured by enzyme-linked immunosorbent assay (ELISA). Endotoxin was determined by a method based on an endotoxin-specific synthetic substrate. Plasma levels of type II PLA2 were significantly higher in the patients who died of sepsis than in those who survived the illness. There was a significant correlation between type II PLA2 and TNF-alpha and IL-6. Type II PLA2, TNF-alpha, IL-6, and IL-8 may be useful as indices of disease severity. The results suggest that TNF-alpha and IL-6 stimulate the production of type II PLA2 in the plasma of patients with sepsis.
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PMID:Plasma levels of type II phospholipase A2 and cytokines in patients with sepsis. 874 87

Knowledge of the aetiology and pathogenesis of the inflammation in ulcerative colitis and Crohn's disease is still insufficient. It is thought that some antigen is the trigger which induces a chain of immune reactions but the origin of this antigen has not so far been elucidated. In theory, an antigen-presenting cell forms a complex with endotoxin-derived peptides as antigen. T-helper lymphocytes recognize this complex, are activated and start to produce cytokines. For inflammatory bowel diseases (IBD) the most important cytokines identified are interleukin 1 (IL-1), interleukin 2 (IL-2), interleukin 6 (IL-6), interleukin 8 (IL-8), gamma-interferon (G-IFN), and tumor necrosis factor-alpha (TNF-alpha). Inhibition of these cytokines can be achieved by administration of cyclosporine, which inhibits the function of T-helper lymphocytes. Orally, intravenously, and locally administered cyclosporine is able to improve the disease activity in ulcerative colitis and Crohn's disease, but its use is limited because of side-effects. The novel immunosuppressant FK506 has comparable actions to cyclosporine in regulating cytokine production and may even be more effective than cyclosporine. The receptor antagonist of IL-1 (IL-1ra) competitively binds to the IL-1 receptor located on several lymphocytes. Treatment of animals with IL-1ra has been successful and clinical trials using recombinant IL-1ra are underway in IBD. Antibodies against alphaIL-2r have also been used successfully in animal studies. No experience with this substance has been obtained in man. The use of alpha-interferon seems to be effective in some patients with Crohn's disease. CD4 and CD8 molecules on lymphocytes are needed to form the interaction between antigen, antigen-presenting cell, and lymphocytes. Specific monoclonal antibodies against CD4 are successfully used in patients with active ulcerative colitis and Crohn's disease. TNF-alpha shares many of the proinflammatory activities of IL-1. In preliminary studies, especially in patients with Crohn's disease, the effects of the administration of antibodies to TNA-alpha were excellent.
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PMID:Selective immunomodulation in patients with inflammatory bowel disease--future therapy or reality? 881 2

The study attempts to evaluate the role of interleukin-6 (IL-6) in the pathogenesis of chronic hepatitis. We have used EIA sensitive methods to determine the serum concentration in patients with chronic active hepatitis of HB (+) (CAH-HE Ag+) antigen, with chronic active hepatitis of HB(-) (CAH-HBAg-) antigen and in those with persistent chronic hepatitis of HB(+) (CPH-HBAg+) antigen, compared with a group of controls (blood donors) in whom HBAgs, antiHBs, HBAge, antiHBe and anti HBc were absent. Disease status diagnosis was given in accordance with international conventions, immunologic tests included. The fact that the T lymphocytes with a CD56 are present in the liver and that same marker is also encountered on the Kuppfer cells, but not on the T lymphocytes in circulation, shows that in the liver the interleukin 6 is produced by the activated T lymphocytes and by the Kuppfer cells. Therefore, in such conditions, LB stimulation and growth is performed rather by IL-6 and to a lesser extent by IL-8. This statement is also supported by the finding that in the lymphocyte cultures in the peripheral blood there is no difference in the response to polyclonal mitogens between patients with CAH-HBAg(+) and those with CAH-HBAg(-). Also, there are no significant differences in the total immunoglobulin concentrations, but there are differences in the IgM concentration (greater in CAH-HBAg(+). In our investigations, the serum level of IL-6 (40.1 +/- 6.8 pg/ml) was higher in those with higher immunoglobulin concentrations-both IgG, but more particularly IgM. The IgM increase was correlated with the presence of HBAg. Therefore, the highest IL-6 values were found in CAH with HBAg(+). Increases of serum IL-6 concentrations were found during intervals of severe hepatic aggression manifested in a cytolitic syndrome, with transaminase increase. In the case of determinations in dynamics, the values decreased as the enzyme titre decreased. We can state that the serum activity of IL-6 reflects the degree of liver inflammation and can be used as a parameter for monitoring the disease.
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PMID:Immune mechanisms in the process of hepatopathies chronicization. Contribution and role of lymphokines. 889 81


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