Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have indicated that airway inflammation in atopic asthma is characterized by T-cell activation and local eosinophilia, but it is unknown whether this also applies to nonatopic asthma. In this study, the cytokine mRNA profile and activation status of inflammatory cells in bronchoalveolar lavage fluid (BALF) of eight nonallergic patients with symptomatic asthma and eight nonallergic healthy controls were compared using the message amplification phenotyping (MAPPing) with the polymerase chain reaction (PCR) procedure and immunocytochemical evaluation. Asthmatics had an increasing number of inflammatory cells in BALF, including activated eosinophils (EG2-positive) (p less than 0.001) and activated T cells (CD25-positive) (p less than 0.001). Activated T cells from five of the eight asthmatic patients and from one control subject expressed high levels of interleukin 5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF). All the asthmatic patients had increased numbers of monocytes in their BALF (p less than 0.002) and those cells invariably showed increased expression of interleukin 1 beta (IL1 beta) transcripts. In five patients they also expressed appreciable levels of IL-6 and GM-CSF mRNA. IL-5 and GM-CSF can induce local activation of eosinophils, and IL-1 beta and IL-6 are known to promote T-cell activation and proliferation. Thus, there is an increased production of cytokines with inflammatory properties in the airways of patients with nonatopic symptomatic asthma, which may contribute to the persistence of inflammation, and monocytes and activated T cells are important sources of these cytokines.
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PMID:Cytokine mRNA profile and cell activation in bronchoalveolar lavage fluid from nonatopic patients with symptomatic asthma. 151 85

The patterns of lymphokine mRNA expression during the development of protective immunity to Mycobacterium leprae after intradermal vaccination of mice with killed M. leprae were studied. Using a polymerase chain reaction-based technique for detecting mRNA expression in small numbers of cells, we observed changes in the mRNA expression of a number of cytokine genes in the lymph nodes draining the site of vaccination. In particular, IL-1 (-alpha and -beta), IL-2, TNF (-alpha and -beta), and IFN-gamma mRNA were readily detected, whereas IL-3, IL-4, IL-5, IL-6, IL-7, and granulocyte-macrophage colony-stimulating factor mRNA were not detected, or were detectable only at very low levels. This is consistent with the selective activation of Th-1 Th cells. The effect of in vitro exposure of these cells to the immunizing Ag was also investigated; again, IL-1, IL-2, TNF, and IFN-gamma mRNA were abundant, but in addition, IL-3, IL-6, and granulocyte-macrophage colony-stimulating factor mRNA were greatly increased, suggesting an important role in the recall response.
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PMID:Role of Th-1 lymphocytes in the development of protective immunity against Mycobacterium leprae. Analysis of lymphocyte function by polymerase chain reaction detection of cytokine messenger RNA. 153 45

Natural suppressor (NS) cells, which nonspecifically suppress immune responses, are present in the spleen following exposure to radiation, chronic graft-versus-host disease, or cancer and in normal bone marrow. A model system is described which allows the study of cytokines activating and inhibiting NS cells, cytokines mediating NS activity, and NS effects on cytokine synthesis. Recombinant interleukin-3 (rIL-3) and granulocyte-macrophage colony-stimulating factor (rGM-CSF) efficiently activated NS cells present in normal bone marrow and were effective at concentrations as low as 5 U/ml. At high concentrations, GM-CSF, but not IL-3, did not activate NS cells. Recombinant interferon-gamma (rIFN-gamma) blocked the activation of bone marrow NS cells by rIL-3, but did not down-regulate NS cells once activated. The NS cells secreted one or more soluble suppressor factors, which blocked IL-2 synthesis and also inhibited IL-2-dependent T cell proliferation in the presence of excess IL-2.
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PMID:Cytokine regulation of bone marrow natural suppressor cell activity in the suppression of lymphocyte function. 153 70

The present results demonstrate that macrophages from mice susceptible to infection with Leishmania mexicana amazonensis sustain a higher production of granulocyte-macrophage colony-stimulating factor (GM-CSF) throughout the in vitro infection than macrophages from a resistant strain. Resident macrophages from BALB/c and C57B1/10 mice were infected with promastigotes of L. mexicana amazonensis and the amount of biologically active GM-CSF was measured in the supernatants collected at different times of infection. Measurements were made by bone marrow and GM-CSF/interleukin-3 addicted cell proliferation. Because GM-CSF is a disease-exacerbating cytokine, its differential production by infected macrophages may be one of the mechanisms defining resistance or susceptibility to a leishmanial infection.
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PMID:Differential production of granulocyte-macrophage colony-stimulating factor by macrophages from mice susceptible and resistant to Leishmania mexicana amazonensis. 154 6

Leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) are multifunctional cytokines with many similar activities. LIF is structurally and functionally related to another cytokine, Oncostatin M (OSM), that binds to the high-affinity LIF receptor but not to the low-affinity LIF receptor. A complementary DNA was isolated that encodes the high-affinity converting subunit of the LIF receptor. The converter conferred high-affinity binding of both LIF and OSM when expressed with the low-affinity LIF receptor and is identical to the signal transducing subunit of the IL-6 receptor, gp130. The gp130 subunit alone confers low-affinity binding of OSM when expressed in COS-7 cells. This receptor system resembles the high-affinity receptors for granulocyte-macrophage colony-stimulating factor, IL-3, and IL-5, which share a common subunit.
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PMID:The IL-6 signal transducer, gp130: an oncostatin M receptor and affinity converter for the LIF receptor. 154 94

To test the hypothesis whether peripheral blood hematopoietic progenitor/stem cells (PBSCs) interact with vascular endothelial cells during events leading to extramedullary hematopoiesis, we cocultured T-cell depleted, peripheral blood mononuclear cells obtained from cytokine treated primates in liquid culture containing a monolayer of porcine aortic endothelial cells (PAECs) for 7 days. Recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) added to cocultures of PBSC-PAEC stimulated colony formation, while only a few clusters were observed in cultures without GM-CSF. In contrast, colony formation was not stimulated when either interleukin 1 (IL-1) or IL-3 were added to the cultures. Colony and cluster formation in response to GM-CSF was dose dependent; 20 +/- 5 colonies/5,000 cells were formed at 3 U/ml, and optimal colony formation of 42 +/- 11/5,000 cells occurred at 100 U/ml. Colonies formed in the presence of GM-CSF were large, and most contained greater than 200 cells. Morphological and phenotypical characterization of cells from isolated colonies suggested that the majority of cells were predominantly immature myeloid elements. However, there was also a low but consistent frequency of megakaryocytic lineage cells. Thus, PBSCs interact with non-bone marrow--derived vascular endothelial cells and proliferate, but only in the presence of GM-CSF, suggesting that PBSC interaction with vascular endothelial cells in vivo could lead to extramedullary hematopoiesis.
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PMID:Peripheral blood hematopoietic progenitor/stem cells proliferate to form colonies in liquid culture but require contact with vascular endothelial cells and GM-CSF. 154 50

Cytokine expression and production by human megakaryocytic cells were studied using the CMK cell line as a model for cytokine gene expression by cell line as a model for cytokine gene expression by polymerase chain reaction (PCR) and for cytokine protein synthesis by specific radioimmunoassays. CMK cells at all stages of maturation were found to constitutively express moderate mRNA levels for tumor necrosis factor (TNF-alpha), transforming growth factor beta (TGF-beta), interleukin (IL) 1 beta, and endothelial cell growth factor (ECGF) transcripts. After 6-h treatment with the phorbol ester PMA, gene expression for IL-1 alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, and the IL-6 receptor were increased. After 24 h of exposure to PMA, levels for most cytokines declined to baseline, except for IL-6 which appeared as a new transcript. PMA-stimulated CMK lines synthesized low levels of TNF-alpha and IL-6, and higher levels of GM-CSF, IL-1 beta, and IL-1 alpha protein. These observations suggest that cells of megakaryocytic lineage are capable of producing a repertoire of cytokines which could mediate an autocrine role as well as modulate the replication and function of other hematopoietic cells.
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PMID:Cytokine gene expression and synthesis by human megakaryocytic cells. 154 52

Freshly isolated human mononuclear cells (5 x 10(6)) were incubated in a Dexter-type long-term bone marrow culture (LTBMC) system to study myelosuppressive effects of cytosine arabinoside (Ara-C) in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin 3 (IL-3). Differential counts (dc) of the nonadherent cell (nac) populations, starting with culture initiation, were performed weekly. After one week of simultaneous incubation of LTBMCs with either cytokine (100 ng/ml) and Ara-C (1 microgram/ml), nac numbers were markedly reduced compared to controls. Dc after week 1 of culture demonstrated significant decreases of all myeloid cell fractions except for macrophages, which remained unaffected. Growth factor-dependent LTBMCs exposed to Ara-C showed recovery of promyelocytic, metamyelocytic, and polymorphonuclear cell numbers up to control values (cultures without Ara-C exposure) in weeks 3 to 6. Intriguingly, high-proliferative, early myeloid progenitor cells (myeloblasts) appeared at high rates only in IL-3-dependent LTBMCs with and without Ara-C exposure. Nac numbers in LTBMCs exposed to Ara-C alone declined rapidly; after two weeks of culture only negligible numbers of viable nac were maintained. Plating experiments of nac in the presence of GM-CSF were performed weekly. Granulocyte-macrophage colony-forming units (CFU-GM) yields for nac from IL-3 LTBMCs were consistently higher than those for nac from GM-CSF LTBMCs. Ara-C exposure reduced CFU-GM numbers generated with nac from GM-CSF LTBMCs to 10% of GM-CSF controls (week 1). However, CFU-GM numbers grown with nac from Ara-C exposed GM-CSF-dependent LTBMCs recovered above control levels after week 3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myelosuppressive effects of cytosine arabinoside (Ara-C) on growth factor-dependent human long-term bone marrow cultures (LTBMC). 155 25

Morphological and immunohistochemical analyses have documented the development of an acute inflammatory response, marked by the early appearance of granulocytes and later infiltration of mononuclear cells, in the uterus immediately after mating in mice. The response peaked on Day 1 and subsided by Day 3. In the present study, RNAs for macrophage colony-stimulating factor (CSF-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and for interleukin 1 alpha (IL-1 alpha), IL-1 beta, interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha) were detected in uterine tissue on Day 1. With the exception of IL-6, which was higher on Day 3 than on Day 1, and IL-1 alpha, which was not reduced on Day 2, concentrations of cytokine mRNA decreased to Day 3. No bioactivity was detected for GM-CSF, granulocyte colony-stimulating factor or IL-3, but CSF-1, IL-1, IL-6 and TNF-alpha were detected on Day 1 using bioassays. Changes in concentrations approximately paralleled those for mRNA. The concentrations of mRNA for CSF-1, IL-1, IL-6 and TNF-alpha were higher on Day 1 of pregnancy than in the uteri of cycling mice 24 h earlier. The data are consistent with previous morphological observations demonstrating the expression of an acute inflammatory response in the mouse uterus after mating. Further, the data demonstrate the expression of genes for CSF-1, GM-CSF, IL-1 alpha, IL-1 beta, IL-6 and TNF-alpha is induced in the uterus during mating.
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PMID:Expression of colony-stimulating factors and inflammatory cytokines in the uterus of CD1 mice during days 1 to 3 of pregnancy. 155 82

Colony-stimulating factor 1 (CSF-1) is a cytokine involved in hematopoiesis and perhaps more importantly in the early stages of immunological defense mechanisms. Although numerous studies of in vitro CSF-1-producing cells have been published, in vivo data is totally lacking. According, we performed immunohistochemical detection of CSF-1-positive cells on frozen sections of reactive lymphadenitis (three cases) and Hodgkin's disease (13 cases) lymph node biopsies, using as antibody a highly specific polyclonal rabbit antiserum prepared in our laboratory. Endothelial cells from high endothelial venules and most fibroblasts were positive in all cases (reactive lymphadenitis and Hodgkin's samples), and most lymphocytes in interfollicular T cell areas showed faint granular positivity in reactive lymphadenitis lymph nodes. Hodgkin and Reed-Sternberg cells were positive in all cases tested, although staining intensity was highly variable and the percentage of positive cells differed from case to case. These data from in vivo biopsies confirm previous results for in vitro CSF-1 production by endothelial cells, fibroblasts, T lymphocytes, and Hodgkin cell lines. They are consistent with the role of this cytokine in immune response and raise the question of its significance in Hodgkin's disease.
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PMID:Immunohistochemical detection of cells positive for colony-stimulating factor 1 in lymph nodes from reactive lymphadenitis, and Hodgkin's disease. 155 43


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