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)

Interleukins (IL) are a heterogeneous class of cytokines involved in activation of T lymphocytes (IL-1, 2, 4, 6 and 7), B lymphocytes (IL-1, 2, 4, 5, 6 and 7), and macrophages (IL-1 and 4), and hematopoiesis (IL-1, 2, 3, 4, 5, 6 and 7), acting either by themselves, or as co-stimulator factors. Interleukin-1 (IL-1 alpha and IL-1 beta) is induced by different signals including microbial products; it mediates various events occurring during inflammation (e.g. fever, osteolysis, leucopenia, hypotension, hyperalgia, etc...). Such mechanisms are often the consequences of the induction by IL-1 of lipid mediators (e.g. prostaglandins, platelet activating factor, etc). IL-1 often acts synergistically with Tumor Necrosis Factor during the pro-inflammatory process. IL-1 as well as microbial products induces the production of interleukin-6 and interleukin-8. IL-6 also plays a role in inflammation, mainly as an inducer of acute phase proteins synthesis by hepatocytes. IL-8 has chemotactic and activating properties for neutrophils.
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PMID:[Interleukins and inflammation]. 230 78

The influence of human monocyte-derived chemotactic peptide (GCP/IL-8) on degranulation of neutrophils was investigated in relation to that of other monokines. GCP/IL-8 promoted a dose-dependent release of lactoferrin from specific granules but had no effect on enzyme release from primary granules. From the other monokines that were tested, tumour necrosis factor alpha (TNF alpha) also induced degranulation, while IL-1 beta and IL-6 scored negatively. TNF alpha-induced lactoferrin release was enhanced by cytochalasin B pretreatment of the granulocytes, while GCP/IL-8-promoted degranulation was not. In contrast to GCP, TNF alpha also caused the release of LDH, suggesting a non-specific cell destruction. These observations further support the view that, unlike the other monokines, GCP/IL-8 is a true and specific granulocyte activator.
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PMID:Human granulocyte chemotactic peptide (IL-8) as a specific neutrophil degranulator: comparison with other monokines. 267 Jul 52

Previous findings provided evidence that bacterial lipopolysaccharide (LPS)-activated human monocytes are able to upregulate autologous polymorphonuclear (PMN) phagocytic ability via cell-to-cell contact mechanisms mediated by membrane (m)-associated cytokines (CKs), such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 alpha, IL-1 beta, IL-6 and IL-8. Consequently, the role of the lymphocyte function-associated antigen (LFA)-1 molecule on the monocyte (Mo)-PMN interplay was evaluated. In the first step, lipid A (LA)-stimulated Mo were pretreated with anti-recombinant human (Rhu) LFA-1 alpha monoclonal antibody (MoAb), and the enhanced phagocytic activity of PMN was abrogated. Pretreatment of unstimulated Mo with the same MoAb led to a reduction of PMN phagocytosis. In the second step, the role of m-LFA-1 on PMN was investigated with regard to Mo modulation. Anti-Rhu LFA-1 alpha MoAb was supplemented to LA-activated and unstimulated PMN, respectively, before coculturing with autologous LA-activated Mo. The addition of anti-Rhu LFA-1 alpha MoAb gave rise to a significant decrease in PMN phagocytosis regardless of PMN activation. These data suggest that, besides m-CKs, LFA-1 present on Mo and PMN might be involved in the mutual interplay between PMN and Mo.
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PMID:Role of lymphocyte function-associated antigen-1 on the interplay between lipid A-activated monocytes and polymorphonuclear cells. 747 67

Neurodegenerative processes in Alzheimer disease (AD) are thought to be driven in part by the deposition of amyloid beta (A beta), a 39- to 43-amino acid peptide product resulting from an alternative cleavage of amyloid precursor protein. Recent descriptions of in vitro neurotoxic effects of A beta support this hypothesis and suggest toxicity might be mediated by A beta-induced neuronal calcium disregulation. In addition, it has been reported that "aging" A beta results in increased toxic potency due to peptide aggregation and formation of a beta-sheet secondary structure. In addition, A beta might also promote neuropathology indirectly by activating immune/inflammatory pathways in affected areas of the brain (e.g., cortex and hippocampus). Here we report that A beta can modulate cytokine secretion [interleukins 6 and 8 (IL-6 and IL-8)] from human astrocytoma cells (U-373 MG). Freshly prepared and aged A beta modestly stimulated IL-6 and IL-8 secretion from U-373 MG cells. However, in the presence of interleukin-1 beta (IL-1 beta), aged, but not fresh, A beta markedly potentiated (3- to 8-fold) cytokine release. In contrast, aged A beta did not potentiate substance P (NK-1)- or histamine (H1)-stimulated cytokine production. Further studies showed that IL-1 beta-induced cytokine release was potentiated by A beta-(25-35), while A beta-(1-16) was inactive. Calcium disregulation may be responsible for the effects of A beta on cytokine production, since the calcium ionophore A23187 similarly potentiated IL-1 beta-induced cytokine secretion and EGTA treatment blocked either A beta or A23187 activity. Thus, chronic neurodegeneration in AD-affected brain regions may be mediated in part by the ability of A beta to exacerbate inflammatory pathways in a conformation-dependent manner.
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PMID:Amyloid beta peptide potentiates cytokine secretion by interleukin-1 beta-activated human astrocytoma cells. 747 75

Sera from 42 patients with rheumatoid arthritis (RA) and 40 healthy controls (HC) were examined for cytokine autoantibodies (CK-aAb) by accurate and sensitive radioimmunoassays. The prevalences of detectable CK-aAb in RA (HC) were: aAb-IL-1 alpha = 36% (38%); aAb-IL-6 = 29% (13%), p = 0.06; aAb-IL-8 = 0% (0%); aAb-IFN alpha = 12% (3%), p = 0.11. The levels of the individual CK-aAb did not correlate, and there were no correlations between CK-aAb levels and clinical or laboratory variables. CK-aAb levels remained constant in 8 RA patients tested over a period of 6 months. With regard to alterations in aAb-IL-1 alpha levels, 4/11 HC were consistently positive over 18-36 months; 2/11 converted and became highly positive. The levels of aAb-IFN alpha and aAb-IL-6, but not aAb-IL-1 alpha, tended to be increased in RA patients; aAb-IL-8 were undetectable in both RA and HC.
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PMID:Cytokine autoantibodies in rheumatoid arthritis. 748 81

The aims of the study were to determine whether the platelet-activating factor antagonist Lexipafant could alter the clinical course and suppress the inflammatory response of human acute pancreatitis. In a double-blind, placebo-controlled study 83 patients were randomized to receive Lexipafant 60 mg intravenously for 3 days, or placebo. Clinical progression was assessed by daily Acute Physiology And Chronic Health Evaluation (APACHE) II score and organ failure score (OFS). The magnitude of the inflammatory response on days 1-5 was assessed by serial measurement of interleukin (IL) 8, IL-6, E-selectin, polymorphonuclear elastase-alpha1-antitrypsin (PMNE-alpha 1-AT), and C-reactive protein (CRP). At entry, patients receiving Lexipafant (n = 42) or placebo (n = 41) were matched for age and sex, aetiology, APACHE II score and OFS. The disease was classified as severe in 29 patients (APACHE II score eight or more). There was a significant reduction in the incidence of organ failure (P = 0.041) and in total OFS (P = 0.048) at the end of medication (72 h). During this time seven of 12 patients with severe acute pancreatitis who had Lexipafant recovered from an organ failure; only two of 11 with severe acute pancreatitis who had placebo recovered from an organ failure and two others developed new organ failure. Lexipafant treatment significantly reduced serum IL-8 (P = 0.038), and IL-6 declined on day 1. Plasma PMNE-alpha 1-AT complexes peaked on day 1; the gradual fall to baseline over 5 days observed in controls did not occur in patients given Lexipafant. No effect was observed on serum CRP. This study provides a rationale for further clinical trials with the potent PAF antagonist Lexipafant in human acute pancreatitis.
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PMID:Randomized, double-blind phase II trial of Lexipafant, a platelet-activating factor antagonist, in human acute pancreatitis. 748 82

A cDNA encoding human IL-17 (hIL-17) was cloned from a CD4+ T cell library. The predicted 155-amino acids sequence contains an N-terminal signal peptide and exhibits 72% amino acid identity with HVS13, an open reading frame from a T-lymphotropic Herpesvirus saimiri, and 63% with murine CTLA8. High levels of hIL-17 were induced from primary peripheral blood CD4+ T cells upon stimulation. When expressed in CV1/EBNA cells, recombinant hIL-17 was secreted in both glycosylated and nonglycosylated forms. A hIL-17.Fc fusion protein and supernatants from cells transfected with hIL-17 induced IL-6 and IL-8 production and enhanced the surface expression of the intracellular adhesion molecule-1 (ICAM-1) in human fibroblasts.
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PMID:Human IL-17: a novel cytokine derived from T cells. 749 28

This paper reviews the mechanisms leading to the commencement of labor in the presence of intrauterine infection. It is postulated that induction of preterm contractions represents an escape mechanism of the fetus from a hostile environment. Bacterial toxins provoke an immunological response (macrophages) of the fetomaternal compartment. Liberation of cytokines (IL-1, IL-6, IL-8) stimulates prostanoid synthesis in the decidua and amnion, as well as migration of granulocytes into the cervix. Additional still unknown factors may determine whether this process leads to cervical dilatation, effacement and finally preterm delivery. The role is discussed of other cytokines, i.e., colony-stimulating factors, transforming growth factor beta, and interleukin receptor antagonists as potential, clinically useful tocolytics in this labile equilibrium.
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PMID:[Intra-amniotic infection, cytokines and premature labor]. 750 7

The effects of irradiation on cytokine production in glioma cell lines, NP1, NP2 and NP3, were studied. Culture supernatants were collected after 6, 24, 48 or 72 hours and the concentrations of interleukin (IL)-6 and IL-8 measured by enzyme-linked immunosorbent assay. Spontaneous and IL-1 beta-stimulated productions were analyzed. Some cells were given a single dose of Lineac irradiation (10 or 20 Gy). Production of IL-6 (with or without IL-1 beta stimulation) increased gradually to a maximum after 72 hours, more in the 20 Gy-irradiated cells than 10 Gy cells (p < 0.01). Production of IL-8 increased gradually to a maximum after 48 or 72 hours. Spontaneous production of IL-8 increased more in 20 Gy-irradiated cells than 10 Gy cells after 6 and 24 hours (p < 0.01), but increased more in 10 Gy cells than 20 Gy cells after 48 and 72 hours (p < 0.01). The production of IL-8 stimulated by IL-1 beta increased more in 10 Gy cells than 20 Gy cells 24 hours later (p < 0.01). IL-6 and IL-8 production differed in the response to irradiation. Our data suggest that bidirectional communication between the immune system and glioma cells changes after radiotherapy.
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PMID:Effects of irradiation on cytokine production in glioma cell lines. 750 9

A large number of cytokines are found within foci of inflammation. Two of these cytokines, namely interleukin-1 (IL-1) and tumor necrosis factor (TNF), play a key role in orchestrating the mechanisms responsible for inflammation. These two cytokines induce production by many cells of lipid mediators, proteases, and free radicals, all of which play a direct role in development of the deleterious effects of inflammation. IL-1 and/or TNF exert cytotoxic effects on the vascular endothelium, cartilage, bone, muscle, or pancreatic beta-cell islets. Cytokines, including interferon gamma (IFN), IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), amplify the inflammatory response by increasing production of IL-1 and TNF by macrophages. Macrophages also produce other cytokines, such as IL-8 and macrophage chemoattractant protein-1 (MCP-1), with chemoattractant properties that contribute to draw leucocytes to the site of inflammation. IL-6, produced in large amounts during inflammatory processes, induces the production of acute phase proteins by hepatocytes. IL-1, TNF, IL-11, leukemia inhibitory factor (LIF), and transforming growth factor beta (TGF beta) share this effect. TGF beta also has a number of anti-inflammatory effects. TGF beta, IL-4, and IL-10 inhibit production of IL-1 and TNF. Glucocorticoids also have this effect. Glucocorticoids can be produced as a result of a chain of events initiated by IL-1, TNF, and IL-6 and involving the neuro-endocrine axis. Other substances, such as IL-1 receptor antagonist (IL-1 ra) or soluble forms of the TNF receptors, can specifically inhibit the effects of IL-1 and TNF. Cascade production of cytokines, inhibition, negative feed-back, and synergistic mechanisms are parameters that illustrate the concept of "cytokine network" and aptly characterize the role of these mediators in the mechanisms of inflammation.
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PMID:[Contribution of cytokines to inflammatory mechanisms]. 750 93


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