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, Chun C. Chao

Research output: Contribution to journalArticlepeer-review

58 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)1137-1140
Number of pages4
JournalJournal of Infectious Diseases
Volume172
Issue number4
DOIs
StatePublished - Oct 1995

Bibliographical note

Funding 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.

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