Linked Life Data

8608807

Source:http://linkedlifedata.com/resource/pubmed/id/8608807

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-5-29
pubmed:abstractText
Tumor necrosis factor (TNF), like granulocyte-macrophage colony-stimul ating factor (GM-CSF), rapidly primed human monocytes for enhanced release of superoxide (O-2) stimulated by receptor-mediated agonists, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and concanavalin A (Con A), but not by phorbol myristate acetate (PMA), which bypasses the receptors to stimulate the cells. The optimal priming was obtained by pretreatment of suspended monocytes with 10 U/mL TNF for 10 minutes at 37 degrees C. The potency of the maximal priming effect was TNF> GM-CSF, and the combined effect of TNF and GM-CSF was greater than that of each cytokine alone. GM-CSF induced an increase in cytoplasmic pH but TNF did not. These findings suggest that TNF and GM-CSF activate monocytes through different mechanisms. TNF and GM-CSF by themselves never triggered O-2 release in suspended monocytes or monocytes adherent to endothelial cells, although both cytokines triggered massive release of O-2 in human neutrophils. In additions, TNF and GM-CSF induced tyrosine phosphorylation of a 42-kD protein in neutrophils but not in monocytes. These findings suggest that the TNF-receptor- or GM-CSF-receptor-mediated signaling pathways for triggering O-(2) release is active in neutrophils but inactive or defective in monocytes. TNF also enhanced phagocytosis of sialidase-treated autologous erythrocytes by monocytes, and this effect was further potentiated in the presence of autologous fresh serum. The significant enhancement of erythrophagocytosis was obtained at 1 U/mL TNF. At this concentration of TNF, the expression of C3bi-receptor (CD11b/CD18) was upregulated. These findings show that TNF rapidly primes human monocytes for enhanced release of O-(2) and erythrophagocytosis and suggest that TNF activates monocytes through autocrine or paracrine mechanisms at the inflammatory sites inasmuch as TNF is primarily produced by activated monocytes/macrophages.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0301-472X
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
559-67
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8608807-Adult, pubmed-meshheading:8608807-Complement C3b, pubmed-meshheading:8608807-Concanavalin A, pubmed-meshheading:8608807-Cytoplasm, pubmed-meshheading:8608807-Erythrocytes, pubmed-meshheading:8608807-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:8608807-Humans, pubmed-meshheading:8608807-Hydrogen-Ion Concentration, pubmed-meshheading:8608807-Monocytes, pubmed-meshheading:8608807-N-Formylmethionine Leucyl-Phenylalanine, pubmed-meshheading:8608807-Phagocytosis, pubmed-meshheading:8608807-Phosphotyrosine, pubmed-meshheading:8608807-Receptors, Leukocyte-Adhesion, pubmed-meshheading:8608807-Recombinant Proteins, pubmed-meshheading:8608807-Superoxides, pubmed-meshheading:8608807-Tetradecanoylphorbol Acetate, pubmed-meshheading:8608807-Time Factors, pubmed-meshheading:8608807-Tumor Necrosis Factor-alpha
pubmed:year
1996
pubmed:articleTitle
Activation of human monocyte functions by tumor necrosis factor: rapid priming for enhanced release of superoxide and erythrophagocytosis, but no direct triggering of superoxide release.
pubmed:affiliation
Department of Cardiology, Jichi Medical School, Tochigi, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't