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)

Monocyte-derived lipid-containing macrophage (MDLM) was the major source of granulomonopoietic enhancing activity (GM-EA) but these well-differentiated cells were unable to synthesize constitutively the granulocyte-macrophage colony-stimulating activity (GM-CSA) that was contributed mostly by the younger monocytoid cells. The presence of various concentrations (0.5-10 micrograms/ml) of lipopolysaccharide (LPS) potentiated the production of GM-EA by MDLM. Enhancement of GM-EA production peaked at about 0.5 micrograms/ml of LPS, but at higher doses (10-40 micrograms/ml) LPS became suppressive. In parallel, LPS-induced production of prostaglandin E2 (PGE2) was observable only at higher doses (10-40 micrograms/ml), suggesting a correlation between PGE2 production and LPS-mediated suppression of GM-EA synthesis. At optimal concentration (0.5 micrograms/ml), LPS could effectively override the inhibitory effect of interferon-gamma on the production of GM-EA. In addition, GM-CSA production by MDLM can be partly restored by stimulation with high doses of LPS (10-40 micrograms/ml). These results suggest that MDLMs have functional potentials similar to the younger macrophages and may play an important role in the regulation of myelopoiesis through the release of GM-EA and related regulators.
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PMID:The effect of lipopolysaccharide on the production of GM-EA, GM-CSA, and PGE2 by human monocyte-derived lipid-containing macrophages. 245 71

Although the genes for four hematopoietic colony-stimulating factors (CSFs) have been cloned, neither the mechanism of the regulation of their production nor their cellular origins have been established with certainty. Monocytes are known to produce colony-stimulating and burst-promoting activities, as well as several monokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). These monokines indirectly stimulate other mesenchymal cells to produce certain colony-stimulating factors such as granulocyte-macrophage CSF (GM-CSF). To determine whether monocytes produce other CSFs and if so, to compare the mechanism of regulation of production with that of endothelial cells and fibroblasts, we investigated the synthesis of CSFs by monocytes, human umbilical vein endothelial cells, and fibroblasts. We used total cellular RNA blot analysis to determine interleukin-3 (IL-3), GM-CSF, granulocyte CSF (G-CSF), and monocyte CSF (M-CSF) messenger RNA (mRNA) content and immunoprecipitation or bioassay to confirm the presence of the specific secreted proteins. The results indicate that M-CSF mRNA and protein are produced constitutively by all three cell types and their level of expression does not increase after induction. In contrast, GM-CSF and G-CSF mRNAs are barely detectable in uninduced monocytes and show an increase in expression after lipopolysaccharide treatment. Retrovirus-immortalized endothelial cells, unlike primary endothelial cells or both primary and immortalized fibroblasts, produce IL-1 constitutively; this correlates with their constitutive production of GM-CSF and G-CSF. IL-3 mRNA was not detectable in any of these cells either before or after induction. The results indicate that these mesenchymal cells can produce three CSFs: GM-CSF, G-CSF, and M-CSF; furthermore, the data suggest that the mechanism of regulation of M-CSF production is different from that of GM-CSF and G-CSF, and that the latter two inducible CSFs are regulated by different factors in monocytes compared with the other mesenchymal cells.
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PMID:Interleukin-1, tumor necrosis factor, and the production of colony-stimulating factors by cultured mesenchymal cells. 245 80

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

Murine bone marrow-derived macrophages (BMM) undergo DNA synthesis in response to growth factors such as colony stimulating factor-1 (CSF-1) and granulocyte-macrophage CSF (GM-CSF). These macrophages can also be "activated," but without subsequent DNA synthesis, by a number of other agents, including lipopolysaccharide (LPS), concanavalin A, zymosan, formyl-methionyl-leucyl-phenylalanine (FMLP), and the Ca2+ ionophore, A23187. When BMM are treated with a range of stimuli, there is some, although not perfect, correlation between transient elevations in both c-myc mRNA and c-fos mRNA levels and increases in DNA synthesis. However, enhanced DNA synthesis and oncogene expression are readily dissociated from rises in inositol phosphates and, by implication, phospholipase C-mediated hydrolysis of phosphatidyl inositol 4,5-bisphosphate. Superoxide formation in BMM can also be dissociated from the other responses and does not necessarily depend on protein kinase C activation.
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PMID:Activation and proliferation signals in murine macrophages: relationships among c-fos and c-myc expression, phosphoinositide hydrolysis, superoxide formation, and DNA synthesis. 255 11

Interleukin-1 (IL-1), a cytokine, primarily produced by monocytes, is the molecule involved in mediating many of the body's responses associated with infection and inflammation. More recently, IL-1 has been shown to sustain elevated levels of circulating granulocytes, stimulate the production of granulocyte-macrophage colony stimulating factors (CSFs) in vitro, increase plasma levels of CSF, and act synergistically with CSFs to increase the number of granulocyte-macrophage progenitors (colony-forming units) (CFU-GM) in vitro. The purpose of this study was to investigate the effect of murine IL-1 on steady-state hematopoiesis in vivo. C3H/HeJ or its normal littermate C3H/HeN male mice were administered either murine recombinant IL-1 at 45, 50, 200, 225, or 900 units (0.0125-0.25 micrograms)/animal, or 200 units (0.05 micrograms) of semipurified IL-1 derived from P388D1 cell culture supernatants. Because one of the responses to IL-1 is increased prostaglandin (PG) production and with the known activity of PGs on hematopoiesis, additional studies incorporated the cyclooxygenase inhibitor indomethacin (IM) (10 mg/kg body weight). In order to study the effect of IL-1 in vivo on pluripotential progenitors (CFU-S), IL-1 was compared with recombinant murine GM-CSF (50, 200, and 900 units; 0.0125, 0.05, and 0.25 micrograms). Control groups consisted of animals receiving either lipopolysaccharide (0.5 mg/kg body weight) or phosphate-buffered saline where appropriate. After 24 h, animals were sacrificed, and their peripheral blood indices and stem cell content of both bone marrow and spleen were evaluated for various committed hematopoietic progenitors: CFU-GM, CFU-Meg, CFU-E, BFU-E, and CFU-DG. Circulating neutrophils were increased following IL-1; however, this increase was reduced following IM. IL-1 marrow-derived CFU-GM, CFU-E, BFU-E, and CFU-Meg were below controls. In contrast, splenic CFU-GM and CFU-Meg were significantly elevated with increasing IL-1 concentrations. Erythroid progenitors were increased following low IL-1 concentrations and reduced in animals receiving IM, thus indicating a role for prostaglandins in the mechanism of IL-1 for influencing hematopoiesis. CFU-DG were increased, however, only when animals were pretreated with IL-1 and their cells implanted into normal hosts, not when normal cells were implanted into animals pretreated with IL-1, indicating a potential target cell effect rather than an indirect, factor-related response.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of murine hematopoiesis in vivo with recombinant murine interleukin-1. 266 87

Purified populations of monocyte, T lymphocyte, and B lymphocyte from normal human peripheral blood were used for the investigation of elaboration/release of granulocyte-macrophage colony-stimulating activity (GM-CSA). Cell separation was performed by a series of techniques including density-cut centrifugation, adhering incubation, carbonyl iron ingestion and E rosette formation. The purity of the isolated cell population was over 95% with a mean viability of 98%. After collection, the cells were resuspended at a concentration of 1 x 10(6)/ml in RPMI-1640 medium containing 5% fetal calf serum and incubated for 7 days at 37 degrees C to prepare conditioned media (CM) for assay of GM-CSA. The results showed that the monocytes could constitutively secrete a considerable amount of GM-CSA, whereas no CSA was produced by T cells or B cells under normal conditions. All the three cell populations released GM-CSA when activated by mitogen stimulation. Monocyte-derived GM-CSA production was greatly enhanced by zymosan (Zym), lipopolysaccharide (LPS) and concanavalin A (Con A), resulting in an augmentation approaching 3 to 4 times the untreated control. For T lymphocytes, the most contributive stimulants to induce GM-CSA release were phytohemagglutinin (PHA) and Con A, while Zym and LPS were not effective. B lymphocytes, after treatment with pokeweed mitogen (PWM) or PHA, were also capable of releasing large amounts of GM-CSA with a peak level near to PHA-stimulated T lymphocytes. The finding suggested that, when activated, B cells may participate in the inflammatory response and in the regulation of granulopoiesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Release of colony-stimulating activity by resting and activated monocytes, T cells and B cells. 267 99

Purified colony-stimulating factor (CSF-1) (or macrophage colony stimulating factor [M-CSF]) stimulated the glucose uptake of murine bone marrow-derived macrophages (BMM) and resident peritoneal macrophages (RPM) as measured by 3H-2-deoxyglucose (2-DOG) uptake. Similar concentrations of CSF-1 stimulated the 2-DOG uptake and DNA synthesis in BMM. Other purified hemopoietic growth factors, granulocyte-macrophage CSF (GM-CSF) and interleukin-3 (IL-3) (or multi-CSF), and the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), even though differing in their mitogenic capabilities on BMM, were also stimulators of 2-DOG uptake in BMM and RPM. The nonmitogenic agents, lipopolysaccharide (LPS) and concanavalin A (Con A), were also active. The inhibition by cytochalasin B and by high concentrations of D-glucose suggest that the basal and stimulated 2-DOG uptake occurred via a carrier-facilitated D-glucose transport system. The responses of the two macrophage populations to the hemopoietic growth factors and to the other agents were quite similar, suggesting that events that are important for the induction of DNA synthesis are not tightly coupled to the earlier rise in glucose uptake. For the BMM, the ability of a particular agent to stimulate glucose uptake did not parallel its ability to promote cell survival. However, stimulation of glucose uptake could still be a necessary but insufficient early macrophage response for cell survival and subsequent DNA synthesis.
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PMID:Activation and proliferation signals in murine macrophages: stimulation of glucose uptake by hemopoietic growth factors and other agents. 283 22

The effect of peritoneal macrophage-conditioned medium (macrophage CM) from lipopolysaccharide-injected mice on granulocyte-macrophage colony (CFU-gm) and megakaryocyte colony (CFU-meg) formation was examined using a plasma clot culture system. Macrophage CM stimulated mouse bone marrow cells to form CFU-gm and CFU-meg in the presence of pokeweed mitogen-stimulated spleen cell-conditioned medium, but it had no effect on colony formation in the absence of exogenous colony-stimulating factors (CSF). CFU-gm and CFU-meg colony formation was enhanced by low concentrations of exogenous GM-CSF or Meg-CSF alone. These data demonstrate that macrophage CM contains an activity that sensitized CFU-gm and CFU-meg to exogenous CSF.
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PMID:Mouse peritoneal macrophages produce CFU-gm and CFU-meg growth-promoting factors. 305 81

The content of macrophage colony-forming cells (M-CFC) and the serum colony-stimulating activity (CSA) were investigated in mice after intravenous administration of Lactobacillus casei YIT9018 (LC9018). In normal BALB/c mice, 500 micrograms of LC9018 increased both femoral and splenic M-CFC; the highest levels were found a few days and a week, respectively, after the administration. LC9018 also induced an increase in splenic M-CFC in C3H/HeJ mice as well as in C3H/HeN mice, unlike lipopolysaccharide (LPS), which was ineffective in C3H/HeJ mice. In Meth A-bearing BALB/c mice, LC9018 (250 micrograms X 5) suppressed the growth of tumor cells and increased femoral and splenic M-CFC to much greater extents than Lactobacillus plantarum YIT0102 (250 micrograms X 5) did. LC9018 induced a rise of serum granulocyte-macrophage CSA in the same way as LPS. Sera taken 6 hr after LPS administration, when transferred to normal mice, induced increases in femoral and splenic M-CFC. However, sera taken 6 hr after LC9018 administration increased neither femoral nor splenic M-CFC. These results indicate that LC9018 modulates myelopoiesis at least at the stage of the proliferation of M-CFC in a different way from LPS, and this ability may be related to its antitumor activity.
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PMID:Induction by Lactobacillus casei of increase in macrophage colony-forming cells and serum colony-stimulating activity in mice. 309 57

The concentrations of tumor necrosis factor (TNF) produced by human peripheral blood mononuclear cells (MNC) were measured using a radioimmunoassay (RIA) for human TNF. This was developed using a rabbit antiserum against human recombinant TNF (Hu rTNF), and Hu rTNF labeled with Na125I by a modification of the chloramine T method. This RIA does not detect human lymphotoxin, interleukin-1 alpha or beta, interleukin 2, interleukin 6, interferon alpha or gamma, granulocyte-macrophage-colony stimulating factor, and C5a des arg. A good correlation (r = 0.89) was found between the RIA and the cytolytic bioassay for TNF. The sensitivity of the RIA is between 3 and 78 pg/ml (median 11 pg/ml). The mean concentration of TNF in 24-h culture supernatants of human MNC exposed to different concentrations of lipopolysaccharide (LPS) was found to increase in dose-dependent fashion and then level off between 50 and 100 ng/ml. The concentrations of IL-1 beta and alpha detected by specific RIAs in these supernatants were between 0.2 and 19 ng/ml and 0.04 and 1 ng/ml, respectively. The amount of TNF produced by human MNC in vitro was determined in a cohort of 50 normal volunteers. Without exogenous stimuli, TNF concentrations were almost always below the detection limit; with 0.5 ng/ml LPS, the median concentration of TNF was 2 ng/ml, and with PHA the median was 3.8 ng/ml. In cultures performed in the presence of indomethacin significantly (p less than 0.005) more TNF was produced. Using this RIA, we could detect TNF in the circulation of mice injected with Hu rTNF. When plasma samples of patients with febrile illnesses were added directly to the RIA, TNF was not detectable, with the exception of patients with malaria. These studies demonstrate the range and sensitivity of LPS-induced and mitogen-induced production of immunoreactive TNF by human MNC in vitro without interference of similar cytokines in bioassays.
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PMID:Concentrations of immunoreactive human tumor necrosis factor alpha produced by human mononuclear cells in vitro. 325 88


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