| RRC ID |
19607
|
| Author |
Noman AS, Koide N, Khuda II, Dagvadorj J, Tumurkhuu G, Naiki Y, Komatsu T, Yoshida T, Yokochi T.
|
| Title |
Thalidomide inhibits lipopolysaccharide-induced nitric oxide production and prevents lipopolysaccharide-mediated lethality in mice.
|
| Journal |
FEMS Immunol Med Microbiol
|
| Abstract |
The effect of thalidomide on lipopolysaccharide-induced nitric oxide (NO) production was studied using RAW 264.7 macrophage-like cells. Thalidomide significantly inhibited lipopolysaccharide-induced NO production via reduced expression of an inducible NO synthase. Thalidomide reduced the phosphorylation of the p65 nuclear factor-kappaB subunit, inhibitory kappaB (IkappaB) and IkappaB kinase in lipopolysaccharide-stimulated cells. However, thalidomide did not affect the expression of interferon-beta (IFN-beta) and interferon regulatory factor-1 in response to lipopolysaccharide. Further, thalidomide inhibited the MyD88 augmentation in lipopolysaccharide-stimulated cells, whereas it did not alter the expression of TIR domain-containing adaptor-inducing IFN-beta in the MyD88-independent pathway. Thalidomide significantly inhibited the NO production in response to Pam(3)Cys, CpG DNA and imiquimod as MyD88-dependent Toll-like receptor (TLR) ligands, but not polyI:C as a MyD88-independent TLR ligand. Therefore, thalidomide was suggested to inhibit lipopolysaccharide-induced NO production via downregulation of the MyD88-dependent signal pathway. The anti-inflammatory action of thalidomide might be involved in the prevention of lipopolysaccharide-mediated lethality in mice.
|
| Volume |
56(3)
|
| Pages |
204-11
|
| Published |
2009-8-1
|
| DOI |
10.1111/j.1574-695X.2009.00567.x
|
| PII |
FIM567
|
| PMID |
19538513
|
| MeSH |
Animals
Cell Line
Cell Survival
Down-Regulation
I-kappa B Kinase / metabolism
I-kappa B Proteins / metabolism
Immunosuppressive Agents / pharmacology*
Lipopolysaccharides / immunology*
Macrophages / drug effects
Macrophages / immunology
Mice
Mice, Inbred C57BL
Myeloid Differentiation Factor 88 / antagonists & inhibitors
Nitric Oxide / antagonists & inhibitors*
Nitric Oxide Synthase / antagonists & inhibitors
Phosphorylation
Survival Analysis
Thalidomide / pharmacology*
Transcription Factor RelA / metabolism
|
| Times Cited |
10
|
|
WOS Category
|
INFECTIOUS DISEASES
MICROBIOLOGY
IMMUNOLOGY
|
| Resource |
| Human and Animal Cells |
RAW 264(RCB0535) |
