Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the mouse gene (G-CSF) encoding granulocyte colony-stimulating factor is controlled by at least three regulatory elements, GPE1, GPE2 and GPE3 (G-CSF promoter elements). A set of 30-mer oligodeoxyribonucleotides (oligos) scanning the GPE3 region (-104 to -51) of the G-CSF promoter was synthesized, and the tetramer of each oligo was inserted upstream from the cat gene with the simian virus 40 enhancer element. By introducing these hybrid genes into human squamous carcinoma CHU-2 and mouse macrophage BAM3 cells, the enhancer core element of the GPE3 was localized to the region from -98 to -79 in the promoter. A nuclear factor which specifically binds to the core element of the GPE3 was constitutively detected in human CHU-2 cells, whereas the expression of a similar, but distinctly different, factor was significantly induced in BAM3 cells by lipopolysaccharide. The results suggest that these nuclear factors play important roles in the constitutive expression of G-CSF in CHU-2 cells and its inducible expression in macrophages.
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PMID:Constitutive and inducible factors bind to regulatory element 3 in the promoter of the gene encoding mouse granulocyte colony-stimulating factor. 128 Feb 41

The kinetics of GM-CSF and G-CSF secretion by purified adherent human monocytes were studied by quantitative immunoassays. Interleukin-1 (IL-1); 4-40 ng/ml and E. coli lipopolysaccharide (LPS); 0.1-1.00 ng/ml, were the most effective stimuli and induced dose-dependent secretion of both GM-CSF and G-CSF. Secretion of newly synthesized CSF was detectable 3-6 hours after stimulation and continued for approximately 24 h. Twenty minutes pulse exposure to LPS was sufficient to induce half maximum secretion of GM-CSF, and after 24-36 h the adherent monocytes could not be restimulated. Neither GM-CSF nor TNF could down-regulate the secretion of GM-CSF. IL-3 induced a minor secretion of GM-CSF whereas TNF, G-CSF, M-CSF and IFN-gamma were unable to induce GM-CSF secretion. In addition to LPS and IL-1, GM-CSF and to a minor degree TNF induced G-CSF secretion. Enriched T lymphocytes secreted GM-CSF, but not G-CSF, after stimulation with PHA or staphylococcal enterotoxin A (SEA), whereas LPS and IL-1 were without stimulatory effects. We also noted that enriched T lymphocytes added to LPS-stimulated adherent monocytes at ratios of 1:10 or more inhibited, in a dose-dependent fashion, GM-CSF secretion by 13-55%. These findings add new quantitative data on CSF secretion by human monocytes.
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PMID:Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) secretion by adherent monocytes measured by quantitative immunoassays. 128 54

Histamine and putrescine (a precursor of polyamines) are formed by histidine decarboxylase (HDC) and ornithine decarboxylase (ODC), respectively. Within a few hours after injection of a lipopolysaccharide (LPS) into mice, HDC is induced in the liver, spleen, lung and bone marrow, and ODC is induced in the liver, spleen and bone marrow. Since LPS is known to stimulate the production of various cytokines, the abilities of various cytokines to induce HDC and ODC in the tissues of mice were examined. IL-2, IL-6, IL-8, IFN gamma and M-CSF were ineffective. IL-1 alpha, IL-1 beta, TNF alpha and TNF beta induced HDC and ODC, as does LPS. On the other hand, GM-CSF and G-CSF induced HDC and ODC only in the spleen and bone marrow within a few hours after their injection. These results suggest that, in addition to their roles in inflammation or immune responses, HDC and ODC are also involved in an early stage of hematopoiesis.
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PMID:GM-CSF and G-CSF stimulate the synthesis of histamine and putrescine in the hematopoietic organs in vivo. 138 20

The colony-stimulating factors (CSF) belong to a group of proteins which regulate blood cell production. Human monocytes allowed to adhere express high levels of M-CSF transcripts and secreted protein at 24 h in the presence but not in the absence of indomethacin (Indo), an inhibitor of prostaglandin E (PGE) production. When induced with lipopolysaccharide (LPS), adherent monocytes express M-CSF, G-CSF, and GM-CSF transcripts and secrete these proteins and TNF. M-CSF and GM-CSF messages increase in LPS-induced monocytes by the addition of Indo, while G-CSF mRNA appears to decrease. Exogenous addition of PGE-2 to LPS-induced monocytes down-modulates the expression of M-CSF and GM-CSF transcripts. G-CSF message is elevated, suggesting an alternate pathway to G-CSF regulation. PGE-2 inhibits the secretion of CSFs and TNF. In contrast, LPS-induced monocytes held 24 h in nonadherent culture express G- and GM-CSF but not M-CSF. Monocytes that are adhered for 24 h and then treated with LPS for an additional 24 h express only M-CSF message and secrete M-CSF and TNF. PGE-2 added with LPS during the 24-48 h induction blocks M-CSF and TNF production, but appears to enhance M-CSF message expression, in contrast to its effect on 0 h inductions. These results suggest that adherence alone induces M-CSF gene expression, but low levels of PGE or other arachidonic acid metabolites limit this expression. Other events in 1 d-cultured monocytes block the ability to induce G-CSF and GM-CSF expression with LPS, and block the suppressive effect of PGE-2 on M-CSF expression at the RNA level.
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PMID:Differential expression of M-CSF, G-CSF, and GM-CSF by human monocytes. 168 60

Superoxide anion (O2-) generation by human blood neutrophils induced by phorbol myristate acetate, formyl-methionyl-leucyl-phenylalanine, and monoclonal antibody YI51 was measured 24 h after incubation in medium alone, medium with recombinant human granulocyte colony-stimulating factor (rG-CSF), and medium with lipopolysaccharide (LPS). Monoclonal antibody YI51 was able to bind to neutrophils and induce O2- generation after the addition of anti-mouse immunoglobulin antibody as a cross-linking agent. In the 24-h culture, there was no significant difference in neutrophil survival among the three cultures. The amount of O2- generated by neutrophils in control medium markedly decreased compared with that before culture. However, cells in medium with rG-CSF or LPS maintained the ability to generate O2- well or moderately, respectively. Thus, the activity maintained by rG-CSF and LPS was neutralized by the anti-G-CSF serum. Furthermore, significant amounts of G-CSF were detected in supernatants of neutrophils cultured with LPS for 24 h. It was not detectable, however, in control supernatants. To examine whether the phenotype of the plasma membrane of cells changed in the 24-h culture, expression of CD16 (FcR III) and YI51 antigens was analyzed by flow cytometry. The expression of CD16 and YI51 antigens on cells cultured with rG-CSF or LPS was maintained compared with that of control cells. These observations thus indicate that G-CSF is one of the factors essential to maintain the functioning and phenotype of mature neutrophils.
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PMID:Recombinant granulocyte colony-stimulating factor and lipopolysaccharide maintain the phenotype of and superoxide anion generation by neutrophils. 169 8

To clarify which cytokines could potentially be produced by astrocytes, we have assessed the presence of mRNA for a number of cytokines in astrocyte-enriched brain cultures. The cultures were derived from neonatal murine brain and were treated with either interferon-gamma, lipopolysaccharide or tumor necrosis factor-alpha, or infected with murine cytomegalovirus. RNA was extracted at 0, 4, 24 and 48 hours post treatment. A DNA copy of total cytoplasmic RNA was synthesised and specific cDNA amplified using the polymerase chain reaction and detected by hybridization with specific probes. The following cytokines were studied: IL3, IL4, IL6, TNF alpha, TGF beta, LIF, G-CSF, M-CSF and GM-CSF. Transcripts for TGF beta, IL6, LIF and M-CSF were present constitutively but increased with stimulation, whereas transcripts for TNF alpha, IL6, GM-CSF, G-CSF and LIF were detected only after stimulation. Messenger RNA for IL3 and IL4 was not detected. The magnitude and kinetics of the induction varied according to the cytokine and the stimulus. These results indicate the possibility of intra-cerebral production of a number of cytokines that may play a role in the clearance of viral or bacterial pathogens and in the generation of neuropathology.
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PMID:Detection of cytokine mRNA in astrocyte cultures using the polymerase chain reaction. 216 30

The macrophage and granulocyte colony-stimulating factors, M-CSF and G-CSF, act in vitro to induce proliferation and differentiation of monocyte and granulocyte progenitor cells, respectively. We show here that both of these CSFs can be produced by stimulated human blood monocytes, but the M-CSF and G-CSF genes are independently regulated. Recombinant human interleukin-3 (IL-3) and GM-CSF primarily induce expression of the M-CSF gene and secretion of M-CSF, whereas bacterial lipopolysaccharide primarily induces expression of the G-CSF gene and secretion of G-CSF. These results suggest that under different conditions of in vitro stimulation the monocyte secretes factors that could lead selectively to either granulocyte or monocyte production.
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PMID:Independent regulation of M-CSF and G-CSF gene expression in human monocytes. 245 27

We have studied the tissue distribution of interleukin (IL) and hemopoietic colony-stimulating factor (CSF) transcripts in mice by S1-nuclease protection analysis. Accumulation of several of these mRNAs in response to intravenous injection of lipopolysaccharide (LPS) appears to occur in a tissue-specific fashion. IL-1 alpha transcripts accumulate in spleen and lung; IL-6 transcripts accumulate in kidney, heart, and spleen; granulocyte-macrophage-CSF transcripts accumulate in lung and heart; and granulocyte-CSF transcripts accumulate in heart. Three distinct patterns of in vivo mRNA accumulation were detected: 1) silent--interleukins 2-5 showed no transcripts in either LPS-treated or untreated animals; 2) induced--IL-1 alpha, IL-6, granulocyte-macrophage (GM)-CSF, and G-CSF transcripts were increased in abundance in LPS-injected mice; and 3) constitutive--M-CSF transcripts were found in similar amounts in both untreated and treated mice and were present in all tissues examined.
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PMID:Tissue distribution of murine hemopoietic growth factor mRNA production. 246 60

Recombinant interleukin (IL) 1 beta and tumor necrosis factor/cachectin (TNF-alpha) induce, usually within 2 h, a dose-dependent increase in the levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF mRNA in cultured human fibroblasts. Maximal induction is reached at about 4-8 h and usually last for at least 48 h. IL 1 beta and TNF have additive effects on the levels of GM- and G-CSF mRNA, and on the secretion of G-CSF activity into the culture medium. IL 1 alpha has the same additive effect that IL 1 beta has with TNF, but no additive effect with IL 1 beta. In contrast, the high basic level of M-CSF (CSF-1) mRNA shows little or lower variations in response to IL 1, TNF-alpha or both IL 1 and TNF-alpha also induce, with similar kinetics, an increase in IL 1 beta but not mRNA level. In contrast to what is observed with macrophages and endothelial cells, E. coli lipopolysaccharide does not modify the fibroblast CSF mRNA level up to 48 h of culture.
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PMID:Interleukin 1 and tumor necrosis factor-alpha additively increase the levels of granulocyte-macrophage and granulocyte colony-stimulating factor (CSF) mRNA in human fibroblasts. 246 2

We investigated normal human mesothelial cells and human malignant mesothelioma cell lines for the ability to produce hematopoietic colony-stimulating factors (CSFs) in culture. Early passage cultures of normal diploid human mesothelial cells spontaneously expressed detectable levels of M-CSF mRNA transcripts, but lacked detectable transcripts for GM-CSF or G-CSF. Exposure of normal mesothelial cells to epidermal growth factor (EGF), lipopolysaccharide (LPS), or tumor necrosis factor (TNF) induced expression of G-CSF mRNA. The combination of EGF and TNF induced threefold more G-CSF transcripts than did either factor alone. GM-CSF transcripts were induced only by the combination of TNF and EGF. Interleukin-1 beta (IL-1 beta) transcripts were induced by EGF, TNF, or LPS and were inhibited by hydrocortisone (HC). All malignant mesothelioma cell lines tested also spontaneously expressed M-CSF transcripts. However, in contrast to normal mesothelial cells, two of four malignant mesothelioma cell lines also autonomously expressed G-CSF and GM-CSF transcripts without TNF, EGF, or LPS stimulation. Secretion of biologically active CSFs was confirmed by testing media conditioned by the various cell types examined. The detection of biologically active CSFs correlated well with the presence of detectable CSF transcripts by Northern analysis. These data indicate that (a) normal human mesothelial cells spontaneously express detectable levels of M-CSF mRNA in culture; (b) EGF is an essential cofactor for optimal induction of G-CSF and GM-CSF expression; (c) exposure of normal mesothelial cells to inflammatory mediators such as LPS and TNF increases the levels of transcripts for CSFs and IL-1 beta; and (d) as compared with normal human mesothelial cells, some cell lines of human malignant mesothelioma exhibit aberrant gene expression for multiple cytokines, including G-CSF, GM-CSF, IL-1 beta, and IL-6.
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PMID:Expression of colony-stimulating factor genes by normal human mesothelial cells and human malignant mesothelioma cells lines in vitro. 278 82


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