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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1990-04-20
    Description: Bacterial lipopolysaccharide (LPS) exerts profound effects on mammalian hosts in part by inducing macrophages to release tumor necrosis factor-alpha (TNF-alpha); the mechanisms involved are unresolved. The microtubule stabilizer taxol shared two actions of LPS on macrophages: it rapidly decreased TNF-alpha receptors and triggered TNF-alpha release. Both actions of taxol were absent in LPS-hyporesponsive C3H/HeJ mice. In recombinant inbred mice, the genes controlling responses to LPS and to taxol were closely linked. Dexamethasone blocked release of TNF-alpha by both stimuli but did not block the decrease in TNF-alpha receptors. Thus, a protein associated with microtubules may be a cellular target of LPS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, A H -- Porteu, F -- Sanchez, E -- Nathan, C F -- CA-43610/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1990 Apr 20;248(4953):370-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Cornell University Medical College, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1970196" target="_blank"〉PubMed〈/a〉
    Keywords: Alkaloids/*pharmacology ; Animals ; Crosses, Genetic ; Dexamethasone/pharmacology ; Lipopolysaccharides/*pharmacology ; Macrophages/*drug effects/metabolism ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Paclitaxel ; Receptors, Cell Surface/*drug effects/metabolism ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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