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.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Infectious Diseases|
|State||Published - Oct 1995|
Bibliographical noteFunding Information:
Received 6 March 1995; revised 5 June 1995. Human brain tissue was obtained under a protocol approved by the Human Subjects Research Committee at our institution. Informed consent was obtained for fetal brain tissue from patients who were undergoing elective abortions. Financial support: National Institutes of Health (DA-04381; lipoarabinomannan provided under contract AI-25147). Reprints or correspondence: Dr. Phillip K. Peterson, Department of Medicine, Hennepin County Medical Center, 701 Park Ave., Minneapolis, MN 55415.