Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes.
Thalidomide selectively inhibits the production of human monocyte tumor necrosis factor alpha (TNF-alpha) when these cells are triggered with lipopolysaccharide and other agonists in culture. 40% inhibition occurs at the clinically achievable dose of the drug of 1 micrograms/ml. In contrast, the amount of total protein and individual proteins labeled with [35S]methionine and expressed on SDS-PAGE are not influenced. The amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony-stimulating factor produced by monocytes remain unaltered. The selectivity of this drug may be useful in determining the role of TNF-alpha in vivo and modulating its toxic effects in a clinical setting.
Sampaio
E P
EP
Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.
Sarno
E N
EN
Galilly
R
R
Cohn
Z A
ZA
Kaplan
G
G
D001798:Blood Proteins / Q000096:biosynthesis / Q000302:isolation & purification; D016207:Cytokines / Q000096:biosynthesis* / Q000097:blood; D004731:Endotoxins / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D008070:Lipopolysaccharides / Q000494:pharmacology; D008970:Molecular Weight; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D012475:Salmonella; D013792:Thalidomide / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D001798:Blood Proteins; D016207:Cytokines; D004731:Endotoxins; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D013792:Thalidomide