Thalidomide inhibits tumor necrosis factor-alpha production by lipopolysaccharide- and lipoarabinomannan-stimulated human microglial cells.
Tumor necrosis factor-alpha (TNF-alpha) is a pathogenic factor in bacterial meningitis. The effect of thalidomide on TNF-alpha 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-alpha release in a dose-dependent manner. The inhibitory effect of thalidomide was similar to that of dexamethasone, although expression of TNF-alpha 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.
Peterson
P K
PK
Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, Minnesota, USA.
Hu
S
S
Sheng
W S
WS
Kravitz
F H
FH
Molitor
T W
TW
Chatterjee
D
D
Chao
C C
CC
D001483:Base Sequence; D001921:Brain / Q000166:cytology; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005333:Fetus / Q000166:cytology; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000032:analysis; D013792:Thalidomide / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000235:genetics
D007166:Immunosuppressive Agents; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C050016:lipoarabinomannan; D013792:Thalidomide; D003907:Dexamethasone