Thalidomide inhibits lipopolysaccharide-induced nitric oxide production and prevents lipopolysaccharide-mediated lethality in mice

Abu Shadat M. Noman, Naoki Koide, Imtiaz I.E. Khuda, Jargalsaikhan Dagvadorj, Gantsetseg Tumurkhuu, Yoshikazu Naiki, Takayuki Komatsu, Tomoaki Yoshida, Takashi Yokochi

研究成果: Article査読

12 被引用数 (Scopus)

抄録

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-κB subunit, inhibitory κB (IκB) and IκB kinase in lipopolysaccharide-stimulated cells. However, thalidomide did not affect the expression of interferon-β (IFN-β) 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-β in the MyD88-independent pathway. Thalidomide significantly inhibited the NO production in response to Pam3Cys, 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.

本文言語English
ページ(範囲)204-211
ページ数8
ジャーナルFEMS Immunology and Medical Microbiology
56
3
DOI
出版ステータスPublished - 08-2009
外部発表はい

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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