UNIPROT:P10145 - FACTA Search

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Query: UNIPROT:P10145 (IL-8)
23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To date no hematopoietic progenitors of dendritic Langerhans' cells (DLC), which represent an highly efficient class of antigen presenting cells, have been identified or the cytokines they elaborate have been defined. Here we describe an acute leukemia patient whose blasts (90-96% in peripheral blood and bone marrow) had a phenotype consistent with putative progenitors of DLC. The patient was treated with ara-C and VP-16 but did not achieve remission. The blasts had lobulated nuclei, no cytoplasmic vacuolation or Auer rods and were weakly positive for acid phosphatase and non-specific esterase and negative for PAS, granzyme A, dipeptidyl aminopeptidase IV, ATPase/ADPase and lysozyme production. The blasts were positive for CD1a, CD4, CD16, CD35, HLADR, HLADQ, CD11b, CD11c, CD14, CD33, CD34, CD11a, CD71, CD19, CD25, IL-2R beta and negative for CD2, CD7, CD8, CD10, CD22, CD56, CD57, surface or cytoplasmic CD3, TCR delta and TCR beta, HTLV-1p19 and P-glycoprotein. On liquid culture with or without 5 x 10(-9) M 12-O-tetradecanoylphorbol-13-acetate (TPA) for 3 days, the blasts formed aggregates of proliferating and elongating cells on the wall of the flasks with a decline in CD34, numerous dendritic processes appeared on the cells and there was strong positivity for ATPase/ADPase, but no other changes in phenotype. No macrophages were observed, indicating derivation from separate DLCs. Cytogenetic analysis showed chromosomal abnormalities and electron microscopy showed Birbeck granules. Southern blotting of DNA showed rearrangement of one allele for both JH and TCR beta but no HTLV-1 related sequences. Culture supernatants from blasts cultured with or without TPA showed the production of large amounts of IL-8, IL-6, TNF-alpha, MIP-1 alpha, IL-10 and interferon gamma and modest amounts of IL-1 alpha, GM-CSF and stem cell factor. The presence not only of CD1a, HLADR, HLADQ and many other characteristics including Birbeck granules, but also differentiation along the lines of DLC with appearance of dendritic processes on the cells and expression of ATPase/ADPase activity, indicate that the leukemic blasts in our patient represented a leukemic counterpart of normal progenitors of DLC and the leukemia a new entity which could possibly be classified as AML-M8. Lastly, many pro-inflammatory cytokines produced by DLC could contribute to inflammation and IL-10 to immunosuppression.
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PMID:Phenotype, genotype and cytokine production in acute leukemia involving progenitors of dendritic Langerhans' cells. 791 55

Increasing evidence suggests an important role for cytokines in the regulation of eosinophilic inflammation. In the present study we investigated the distribution of leukocytes, lymphocyte subsets, their activation state, and the cytokine profile present in BAL fluid from patients with various lung diseases associated with eosinophilia. For this purpose, we analyzed the levels of IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-8, GM-CSF, TNF-alpha, and IFN-gamma, as well as soluble IL-2 and TNF receptors, in concentrated bronchoalveolar lavage (BAL) fluid obtained from clearly defined patients with allergic and nonallergic asthma, eosinophilic pneumonia, allergic bronchopulmonary aspergillosis (ABPA), hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis. BAL fluid from normal individuals and sarcoidosis patients was analyzed as noneosinophilic controls. BAL cytokine levels were compared with the cellular infiltrate and the activation state of CD4+ and CD8+ T cells as measured by the expression of IL-2 receptors (CD25), HLA-DR, and the very late activation antigen VLA-1. Beside the characteristic leukocyte infiltrate in the various lung diseases, all patients demonstrated significantly increased numbers of activated CD4 and CD8 T cells compared with normal individuals. The analysis of the cytokine profile present in BAL fluid revealed a T helper type 2 (Th2) cell cytokine pattern, with elevated IL-4 and IL-5 but normal levels of IL-2 or IFN-gamma in allergic asthma. ABPA patients demonstrated significantly increased levels of IL-4 and IL-5, with low but significantly elevated concentrations of IL-2 and IFN-gamma. In contrast, the analysis of the cytokine profile in sarcoidosis patients revealed a Th1 cell cytokine pattern characterized by increased concentrations of IL-2 and IFN-gamma but normal levels of IL-4 or IL-5. All other patient groups showed a cytokine pattern incompatible with a pure Th1 or Th2 cell response, because IL-5, IL-2, and IFN-gamma were found to be significantly increased. The BAL fluid analysis of the other, mainly non-T cell-derived cytokines and soluble receptors showed increased levels in all patients compared with normal individuals and may represent the ongoing inflammatory responses. In conclusion, whereas increased IL-4 levels were found only in diseases characterized by increased IgE production, IL-5 was elevated in all patients with increased numbers of eosinophils. The close correlation between IL-5 levels, number of eosinophils, and activated T cells further supports a role for IL-5 in causing tissue eosinophilia.
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PMID:Activated T cells and cytokines in bronchoalveolar lavages from patients with various lung diseases associated with eosinophilia. 792 34

In recent studies, sputum smear cell counts were found to be reproducible and usefully applied to research in asthma and other airway conditions. However, cell definition on the smears is poor, and the procedure is tedious and has limited utility. The objective of this study is to improve the methods of sputum examination. The subjects used in this study were people with bronchitis or asthma from whom sputum could be obtained. By inverted microscopy, portions of fresh sputum were selected to exclude salivary contamination. These portions were exposed to different volumes of dithiothreitol for varied time intervals. We used the resulting cell suspensions to perform total cell counts and prepare cytospins for differential cell counts and immunohistochemical stains for GM-CSF, EG2, TNF alpha and IL-8. Cytospins were compared with smears for differential cell counts on the same sputum specimens. Excellent cell dispersion and definition in cytospins could be observed. The time required for differential cell counting on cytospins was reduced and cytospin counts were more reproducible than smears. Greater duration of treatment of sputum with dithiothreitol tended to increase total cell counts and significantly decreased EG2 staining but had no effect on differential cell counts or the cytokine cell components. Therefore the proposed method of sputum examination involving cell dispersion and use of cytospins overcomes a number of the disadvantages of the examination of smears.
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PMID:The evaluation of a cell dispersion method of sputum examination. 798 18

IL-4, a product of the T-helper 0 (Th0) and 2 (Th2) subset, was originally described as a B-cell stimulatory factor and has subsequently been found to suppress IL-1 alpha, IL-1 beta, IL-6, IL-8, and TNF-alpha gene expression in monocytes stimulated with LPS, and to upregulate IL-1 receptor antagonist (IL1-RA) gene expression. In this study we investigated the effect of IL-4 on the expression of cytokine genes in monocytes evoked by other T-helper cell cytokines: IL-2, IL-3, and GM-CSF. IL-4 down-regulated mRNA accumulation of the proinflammatory cytokines IL-1 beta, IL-8, and TNF-alpha in monocytes stimulated with IL-2, IL-3, and GM-CSF. IL-4 also suppressed the IL-2-induced IL-6 mRNA expression. Temporal analysis of the IL-4 down-regulatory effect on the IL-2-, IL-3-, or GM-CSF-induced proinflammatory cytokine gene expression in monocytes provided evidence that IL-4 acts predominantly on the post-transcriptional level. This was supported by the observation that the down-regulatory capacity of IL-4 appeared to be dependent on de novo protein synthesis. IL-4 did not exert significant influence on the induction of expression of IL-1-RA or various CSFs by IL-2, IL-3, and GM-CSF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:IL-4 down-regulates IL-2-, IL-3-, and GM-CSF-induced cytokine gene expression in peripheral blood monocytes. 803 34

Sarcoidosis is a disorder of unknown etiology characterized, pathologically, by the presence of granuloma. Recent advances in cellular and molecular biology have provided new avenues to assess mechanisms of granuloma formation. Cytokine and growth factors, produced and discharged from alveolar macrophages or T cells, are considered to have significant roles in the process of granuloma formation. To investigate the role of such cytokines in sarcoidosis, we examined the expression of them in bronchoalveolar lavage cells at mRNA levels. We applied reverse transcription-polymerase chain reaction (RT-PCR) technique to estimate the amount of mRNA of each cytokine. From the RT-PCR analysis, TNF-alpha, IL-6, PDGF-B and GM-CSF were considered to play an important role at the local alveolar site of sarcoidosis. And TNF-alpha, IL-6, PDGF-B and IL-8 might form the cytokine network at the pulmonary inflammatory site of sarcoidosis.
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PMID:[Role of cytokines from BAL cells in granuloma formation]. 804 25

Langerhans cell histiocytosis (LCH) is characterised by an accumulation of cells ('LCH cells') with the same phenotypic features as normal Langerhans cells found in skin and other organs. The pathogenesis of LCH is unknown but there is increasing evidence to implicate the involvement of lymphokines and proinflammatory cytokines in the tissue damage seen in this disorder. Apart from histiocytes, the lesions contain giant cells, macrophages, neutrophils, eosinophils, lymphocytes, plasma cells and occasional mast cells that are the hallmark of an inflammatory process. The role of cytokines in the recruitment of haemopoietic cells within inflammatory lesions has only recently been recognised. In this article, we review the possible role of cytokines in the pathogenesis of LCH, and provide an overview of the methods currently used to detect and quantitate them. An appreciation of the type, distribution and amount of different cytokines released within lesions can provide clues to the possible aetiology of LCH. Using immunoassays, in situ hybridisation and RT-PCR, increased amounts of IL-1, IL-3, IL-4, IL-8, GM-CSF, TNF alpha, TGF beta and LIF have been demonstrated in LCH lesions. Lymphocytes constitutively produce GM-CSF and IL-3 and, to a lesser degree, IL-1, IL-4 and LIF whilst histiocytes produce TNF alpha, IL-1 beta and GM-CSF.
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PMID:The role of cytokines in the pathogenesis of Langerhans cell histiocytosis. 807 4

We characterized the immunophenotype as well as functional properties--phagocytosis, the uptake of acetylated LDL, and the expression of HLA class II antigens, adhesion molecules, and cytokine mRNA--of fibroblast-like synoviocytes from rheumatoid arthritis synovium. Skin fibroblasts (FB) and umbilical vein endothelial cells (HUVEC) were studied in parallel. Cytofluorometric immunophenotyping by use of 84 mAb and 2 lectins and immunofluorescence microscopy indicated a high degree of homology between the three cell types. Only staining with mAb to von Willebrand factor (vWF) and CD31 and the lectin UEA-I appeared specific to HUVEC, whereas the mAb 5B5 to prolyl 4-hydroxylase that has been reported to be specific to FB stained HUVEC as well as synoviocytes and FB. All of the cells phagocytosed fluorescent latex beads of 1.7 and 2.6 microns in size. The uptake of acetylated LDL could be shown by HUVEC and, surprisingly, by synoviocytes, but not by FB. The induction of HLA-DR, -DP, and -DQ by IFN-gamma on the three cell types showed a similar dose-dependence. The upregulation of ICAM-1 by IL-1 alpha, TNF-alpha, and IFN-gamma appeared similar, whereas the induction of VCAM-1 by IL-1 alpha, IL-4, TNF-alpha, and IFN-gamma showed differences between the three cell types. ELAM-1 was expressed only on HUVEC after treatment with IL-1 alpha and TNF-alpha. The capacity of the cells to produce cytokines was studied at the level of mRNA by reverse transcription and PCR. All three cell types expressed the mRNA of IL-1 alpha, IL-6, IL-8, GM-CSF, and TGF-beta 1 spontaneously or after LPS stimulation, but never TNF-alpha mRNA. Our results indicate a high degree of relationship between the three cell types. In contrast to HUVEC, none of the markers and functional properties investigated appear specific to FB. Therefore, the issue of the origin of fibroblast-like synoviocytes and the role of vascular endothelial cells in the inflamed synovium is discussed.
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PMID:Characterization of the immunophenotype and functional properties of fibroblast-like synoviocytes in comparison to skin fibroblasts and umbilical vein endothelial cells. 808 88

The effect of the chemotactic cytokine, IL-8, on neutrophil function was compared with that of of other cytokines, GM-CSF, G-CSF TNF alpha and IFN-gamma. IL-8 rapidly stimulated a three-fold enhancement of the fMLP-stimulated respiratory burst, but this priming effect was transient compared with the slower and sustained effects of GM-CSF and IFN gamma. Apart from G-CSF, IL-8 was the weakest priming agent and was weaker than GM-CSF in priming arachidonic acid metabolism stimulated by calcium ionophore. When incubated in combination, IL-8 and TNF alpha were highly synergistic in their effects on respiratory burst priming, whereas IL-8 and GM-CSF showed little synergy. In contrast, IL-8 was as potent as GM-CSF at increasing the expression of neutrophil chemotactic peptide receptors and the beta 2 integrin, CD11b. The latter was maximally upregulated within 5 min of stimulation with IL-8, whereas the effect of GM-CSF was much slower. The kinetics of neutrophil respiratory burst priming by IL-8 were the same when measured in whole blood samples and in purified cell suspensions, and IL-8 dose-response curves were similar, showing that the low affinity IL-8 receptors on erythrocytes do not rapidly sequester circulating IL-8. The data suggest that IL-8 plays a minor role in priming neutrophil function and that a more major activity is the regulation of neutrophil adhesion and migration.
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PMID:The effects of interleukin-8 on neutrophil fMetLeuPhe receptors, CD11b expression and metabolic activity, in comparison and combination with other cytokines. 810 74

Neuroblastoma cells in response to retinoic acid (RA) exhibit differentiation. RA, which can promote tumor cell differentiation, has also been shown to regulate tumor-infiltrating leukocytes. In an attempt to explore the relationship between RA-induced neuroblastoma cell differentiation and leukocyte chemotaxis, we investigated expression of IL-1 beta, IL-8, granulocyte-macrophage colony stimulating factor, and tumor necrosis factor-alpha in the undifferentiated and RA-induced differentiated neuroblastoma cells. Using SK-N-SH neuroblastoma cells, we found that RA induced differentiation of SK-N-SH cells as demonstrated by down-regulation of N-myc gene expression, cell-cycle arrest in G1 phase, and phenotypic change. Neither RA-treated nor untreated neuroblastoma cells expressed IL-1 beta, granulocyte-macrophage colony stimulating factor, or tumor necrosis factor-alpha mRNA. RA-treated but not untreated SK-N-SH cells expressed IL-8 mRNA in a time- and dose-dependent fashion. As determined by ELISA, IL-8 levels were detectable in the culture supernatants from RA-treated, but not untreated, neuroblastoma cells (2.65 +/- 0.43 versus 0.05 +/- 0.04 ng/mL). Using neutrophil and lymphocyte chemotactic assays, we found that RA-treated but not untreated culture supernatants of neuroblastoma cells promoted neutrophil and lymphocyte chemotaxis. The RA enhancement of neuroblastoma cell-mediated leukocyte chemotaxis was significantly blocked by anti-IL-8 neutralizing antibodies. These results suggest that RA-induced neuroblastoma cell differentiation is associated with production of functional IL-8, which may be involved in the leukocyte infiltration and activation resulting in tumor regression.
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PMID:Induction of interleukin-8 expression in neuroblastoma cells by retinoic acid: implication of leukocyte chemotaxis and activation. 810 82

Hematopoiesis is regulated by colony-stimulating factors (CSF) and many other cytokines. T helper cell and monocyte/macrophage interactions that take place in the immune response, resulting in the production of many cytokines, probably can influence inducible hematopoiesis. We investigated the effect of the T helper cell-derived lymphokines IL-2, IL-3, GM-CSF, and IFN-gamma, on the expression of cytokine genes in monocytes and compared this to LPS-induced cytokine gene expression in monocytes. To avoid inadvertent activation of monocytes, cells were purified by elutriation and cultured under serum-free, LPS-free, and nonadherent conditions. Similar to LPS, IL-2, IL-3, and GM-CSF induced the expression of IL-1 beta, IL-6, IL-8, TNF-alpha, and IL-1-RA genes in monocytes, but with some differences in the amount and kinetics of cytokine mRNA accumulation. Unlike LPS, IL-2, IL-3, and GM-CSF did not induce G-CSF and GM-CSF gene expression in monocytes. GM-CSF and IL-3 were the only inducers capable of expressing the M-CSF gene in monocytes. IL-2, IL-3, and GM-CSF showed no effect on the IL-10 gene while IFN-gamma appeared to have no effect on any of the cytokine genes studied in monocytes. These data indicate that in the immune response expression of the proinflammatory cytokine genes, IL-1 beta, IL-6, IL-8, and TNF-alpha, can occur and that autoregulatory control mechanisms, like the expression of IL-1-RA gene, are also activated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulatory effects of T cell lymphokines on cytokine gene expression in monocytes. 812 62

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