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Thalidomide Inhibits Tumor Necrosis Factor-α Production by Lipopolysaccharide-and Lipoarabinomannan-Stimulated Human Microglial Cells
Phillip K. Peterson, Shuxian Hu, Wen S. Sheng, Frederic H. Kravitz, Thomas W. Molitor, Delphi Chatterjee and Chun C. Chao
The Journal of Infectious Diseases
Vol. 172, No. 4 (Oct., 1995), pp. 1137-1140
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30133628
Page Count: 5
You can always find the topics here!Topics: Cell culture techniques, Microglia, Messenger RNA, Meningeal tuberculosis, Necrosis, Mycobacterium tuberculosis, Tumors, Macrophages, Cell lines, Neurons
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Tumor necrosis factor-α (TNF-α) is a pathogenic factor in bacterial meningitis. The effect of thalidomide on TNF-α production by microglia, the resident macrophages of the brain, was evaluated. In primary human fetal microglial cell cultures stimulated with lipopolysaccharide or lipoarabinomannan, thalidomide inhibited TNF-α release in a dose-dependent manner. The inhibitory effect of thalidomide was similar to that of dexamethasone, although expression of TNF-α mRNA in microglial cells was reduced only by thalidomide. The results of this in vitro study suggest that thalidomide could have therapeutic potential in gram-negative bacterial and tuberculous meningitis.
The Journal of Infectious Diseases © 1995 Oxford University Press