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)

Levels of cytokines, interleukin (IL)-1 alpha, IL-1 beta, tumor necrosis factor (TNF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were investigated in samples of the middle ear effusions (MEEs) from 144 ears with otitis media with effusion (OME) by enzyme-linked immunosorbent assay, followed by cytologic analysis. Middle ear effusions of the acute purulent type contained a significantly higher concentration of cytokines compared with normal control sera (p < .001). Cytokines were observed at lower levels in MEE in adults than in children. Tests of children at the chronic stage of MEE showed higher levels of TNF than IL-1 and GM-CSF. Meanwhile, IL-1 beta showed significantly higher concentrations in acute purulent types than in serous and mucoid types (p < .01). In cytologic analysis, the mean level of IL-1 beta was significantly higher in the neutrophil-rich group than in other groups (p < .05). Cytokines possess several biologic properties, some of which are associated not only with acute otitis media but also with chronic otitis media. This study showed that cytokines, especially IL-1 beta, contribute to infiltration into the middle ear by inflammatory cells. This implies that the persistent presence of cytokines in MEE could be a factor in prolonged OME.
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PMID:Immunologic characteristics of cytokines in otitis media with effusion. 141 48

A 12-month-old boy with Kostmann's syndrome was admitted with cavitary pulmonary disease. He had also had bacterial conjunctivitis, periorbital cellulitis, pneumonitis, and otitis media since the age of 10 days. His umbilical cord had not fallen off until he was 3 weeks old. Neutropenia was diagnosed at 4 weeks of age. Antineutrophil antibody studies were negative. A bone marrow aspirate showed granulocytic hypoplasia and a maturation arrest at the promyelocyte stage. Hematopoietic cell culture showed normal numbers of colony-forming units-granulocyte macrophage. Serum granulocyte-macrophage colony-stimulating factor level, was 0.24 ng/mL (normal, greater than 0.05 ng/mL). Serum granulocyte colony-stimulating factor levels, measured by enzyme immunoassay, were undetectable. The patient was successfully treated with filgrastim (granulocyte colony-stimulating factor), with an increase in the absolute neutrophil count to 10.0 x 10(9)/L. Thus, our case of Kostmann's syndrome appears to represent a defect in regulation or production of granulocyte colony-stimulating factor.
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PMID:Measurement of serum granulocyte colony-stimulating factor in a patient with congenital agranulocytosis (Kostmann's syndrome). 171 5

We present a seven-month-old boy referred to our hospital with a history of recurrent suppurative infections starting in his neonatal period. Anemia, absolute neutropenia absolute neutrophil count (ANC: 500 cells/microl), pneumonia, purulent otitis media and maturational arrest of granulocytes at promyelocyte-myelocyte level in bone marrow were detected on his admission. He was diagnosed as Kostmann syndrome and recombinant human granulocyte colony-stimulating factor (rhG-CSF) therapy was started at a dose of 10 microg/kg/d, gradually increasing up to 120 microg/kg/d in sequential seven-day courses. As there was no response, rhG-CSF was stopped and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) was started subcutaneously with 2.5 microg/kg/d and was escalated by doubling the dose every seven days to 20 mg/kg/d. By this therapy absolute neutrophil count (ANC) transiently reached above 500 cells/microl, but eosinophilia developed with a total white cell count of 88.200 cells/microl, and a differential count showing 86 percent eosinophils. Since eosinophilia of this magnitude has deleterious effects, and neutrophil production did not significantly increase, we tried combined therapy with rhG-CSF and rhGM-CSF at doses of 10-20 microg/kg/d and 5-10 microg/kg/d, respectively, without any effect on absolute neutrophil count. The patient succumbed from sepsis eight months after the diagnosis.
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PMID:Failure of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor in a patient with Kostmann syndrome. 1077 Jun 86

Inflammation in the middle ear mucosa, which can be provoked by different primary factors such as bacterial and viral infection, local allergic reactions and reflux, is the crucial event in the pathogenesis of otitis media with effusion (OME). Unresolved acute inflammatory responses or defective immunoregulation of middle inflammation can promote chronic inflammatory processes and stimulate the chronic condition of OME. Cytokines are the central molecular regulators of middle ear inflammation and can switch the acute phase of inflammation in the chronic stage and induce molecular-pathological processes leading to the histopathological changes accompanying OME. In this review we present cytokines identified in otitis media, immunoregulatory [interleukin (IL)-2, IL-10, transforming growth factor-beta]) and allergy associated (IL-4, IL-5, granulocyte-macrophage colony-stimulating factor), as crucial molecular regulators, responsible for chronic inflammation in the middle ear and the chronic condition of OME.
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PMID:The immunoregulatory and allergy-associated cytokines in the aetiology of the otitis media with effusion. 1520 48

Cytokine and cellular patterns of effusions may reflect stages of middle ear inflammation. The local interplay between IL-2 and -4 is likely to play a crucial role in the switching of inflammation in the chronic stage. The T-helper cell 2 (Th2) cytokines IL-4, -5 and -13 and the Th2/Th1 cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) regulate the cellular and molecular processes of chronic inflammation in the middle ear and therefore the chronic condition of otitis media with effusion (OME). Early identification of the cytokine and cellular patterns of effusions can be helpful in directing the clinical treatment of OME.We hypothesized that IL-2 and the group of Th2 cytokines regulate chronic inflammation in the middle ear and chronic OME. Effusions from children with persistent OME were analysed to determine the presence of cytokines (the Th1 cytokine IL-2, the Th2 cytokines IL-4, -5 and -13 and the Th1/Th2 cytokine GM-CSF), inflammatory cells (CD4+ T cells, eosinophils, macrophages and neutrophils) and mucin. Cytokines were evaluated by means of a quantitative "sandwich"-type ELISA, inflammatory cells by means of alkaline phosphatase-anti-alkaline phosphatase immunocytostaining and mucin by means of a modified periodic acid-Schiff method based on a slot-blot technique. The cytokine pattern in effusions varied from patient to patient. GM-CSF correlated positively and IL-4 inversely with IL-2 and the increased level of IL-4 may have had an inhibitory effect on IL-2. IL-5 and -13 correlated with IL-4. Inflammatory cells correlated with cytokines as follows: CD4+ T cells with IL-2 and -4; macrophages and neutrophils with GM-CSF; and eosinophils with IL-5. Some cytokine-cellular correlations in effusions were reflected at the clinical level. The mucin content of effusions correlated with the concentrations of IL-4 (>10 pg/ml) and -13, suggesting involvement of IL-4 and -13 in upregulation of the middle ear mucin metabolism.
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PMID:Evidence of T-helper cell 2 cytokine regulation of chronic otitis media with effusion. 1629 84