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Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor- production via down-regulation of MyD88 expression
Abu Shadat M. Noman
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Naoki Koide
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Ferdaus Hassan
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Imtiaz I.-E-Khuda
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Jargalsaikhan Dagvadorj
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Gantsetseg Tumurkhuu
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Shamima Islam
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Yoshikazu Naiki
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Tomoaki Yoshida
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
Takashi Yokochi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan, yokochi{at}aichi-med-u.ac.jp
The effect of thalidomide on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)- production was studied by using RAW 264.7 murine macrophage-like cells. Thalidomide significantly inhibited LPS-induced TNF- production. Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)- and IKK-β Moreover, thalidomide inhibited LPS-induced phosphorylation of AKT, p38 and stress-activated protein kinase (SAPK)/JNK. The expression of myeloid differentiation factor 88 (MyD88) protein and mRNA was markedly reduced in thalidomide-treated RAW 264.7 cells but there was no significant alteration in the expression of interleukin-1 receptor-associated kinase (IRAK) 1 and TNF receptor-associated factor (TRAF) 6 in the cells. Thalidomide did not affect the cell surface expression of Toll-like receptor (TLR) 4 and CD14, suggesting the impairment of intracellular LPS signalling in thalidomide-treated RAW 264.7 cells. Thalidomide significantly inhibited the TNF- production in response to palmitoyl-Cys(RS)-2,3-di(palmitoyloxy) propyl)-Ala-Gly-OH (Pam3Cys) as a MyD88-dependent TLR2 ligand. Therefore, it is suggested that thalidomide might impair LPS signalling via down-regulation of MyD88 protein and mRNA and inhibit LPS-induced TNF- production. The putative mechanism of thalidomide-induced MyD88 down-regulation is discussed.
Key Words: Thalidomide • LPS • TNF- • MyD88 • RAW 264.7 cells
References
- Hideshima T., Chauhan D., Schlossman R. et al. The role of tumor necrosis factor- in the pathophysiology of human multiple myeloma: therapeutic applications. Oncogene 2001; 20: 4519-4527.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Eisen T., Boshoff C., Mak I. et al. Continuous low dose thalidomide: a phase II study in advanced melanoma, renal cell, ovarian and breast cancer. Br J Cancer 2000; 82: 812-817.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Corral LG, Haslett PA, Muller GW et al. Differential cytokine modulation and T cell activation by two distinct classes of thalidomide analogs that are potent inhibitors of TNF-alpha. J Immunol 1999; 163: 380-386.[Abstract/Free Full Text]
- Haslett PA, Corral LG, Albert M. et al. Thalidomide costimulates primary human T lymphocytes, preferentially inducing proliferation, cytokine production, and cytotoxic responses in the CD8+ subset. J Exp Med 1998; 187: 1885-1892.[Abstract/Free Full Text]
- Zwingenberger K., Wnendt S. Immunomodulation by thalidomide: systematic review of the literature and of unpublished observations. J Inflamm 1995; 46: 177-211.[Web of Science][Medline]
[Order article via Infotrieve]
- Sampaio EP, Sarno EN, Galilly R. et al. Thalidomide selectively inhibits tumor necrosis factor-alpha production by stimulated human monocytes. J Exp Med 1991; 173: 699-703.[Abstract/Free Full Text]
- Moreira AL, Sampaio EP, Zmuidzinas A. et al. Thalidomide exerts its inhibitory action on tumor necrosis factor-alpha by enhancing mRNA degradation. J Exp Med 1993; 177: 1675-1680.[Abstract/Free Full Text]
- Paul SC, Lv P., Xiao YJ et al. Thalidomide in rat liver cirrhosis: blockade of tumor necrosis factor-alpha via inhibition of degradation of an inhibitor of nuclear factor-kappaB. Pathobiology 2006; 73: 82-92.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Ishikawa M., Kanno S., Takayanagi M. et al. Thalidomide promotes the release of tumor necrosis factor-alpha (TNF-alpha) and lethality by lipopolysaccharide in mice. Biol Pharm Bull 1998; 21: 638-640.[Web of Science][Medline]
[Order article via Infotrieve]
- Kawai T., Adachi O., Ogawa T. et al. Unresponsiveness of MyD88-deficient mice to endotoxin. Immunity 1999; 11: 115-122.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Shakhov AN, Collart MA, Vassalli P. et al. Kappa B-type enhancers are involved in lipopolysaccharide-mediated transcriptional activation of the tumor necrosis factor alpha gene in primary macrophages. J Exp Med 1990; 171: 35-47.[Abstract/Free Full Text]
- Saklatvala J., Davis W., Guesdon F. Interleukin 1 (IL1) and tumour necrosis factor (TNF) signal transduction. Philos Trans R Soc Lond B Biol Sci 1996; 351: 151-157.[Abstract/Free Full Text]
- Han J., Lee JD, Bibbs L. et al. A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. Science 1994; 265: 808-811.[Abstract/Free Full Text]
- Hambleton J., Weinstein SL, Lem L. et al. Activation of c-Jun N-terminal kinase in bacterial lipopolysaccharide-stimulated macrophages. Proc Natl Acad Sci USA 1996; 93: 2774-2778.[Abstract/Free Full Text]
- Herrera-Velit P., Reiner NE Bacterial lipopolysaccharide induces the association and coordinate activation of p53/56lyn and phosphatidylinositol 3-kinase in human monocytes. J Immunol 1996; 156: 1157-1165.[Abstract]
- Chakravortty D., Kato Y., Sugiyama T. et al. The inhibitory action of sodium arsenite on lipopolysaccharide-induced nitric oxide production in RAW 267.4 macrophage cells: a role of Raf-1 in lipopolysaccharide signaling. J Immunol 2001; 166: 2011-2017.[Abstract/Free Full Text]
- Naiki Y., Michelsen KS, Zhanq W. et al. Transforming growth factor-β differentially inhibits MyD88-dependent, but not TRAM-and TRIF-dependent, lipopolysaccharide-induced TLR4 signaling. J Biol Chem 2005; 280: 5491-5495.[Abstract/Free Full Text]
- Keifer JA, Guttridqe DC, Ashburner BP et al. Inhibition of NF-kappa B activity by thalidomide through suppression of IkappaB kinase activity. J Biol Chem 2001; 276: 22382-22387.[Abstract/Free Full Text]
- Zandi E., Rothwarf DM, Delhase M. et al. The IkappaB kinase complex (IKK) contains two kinase subunits, IKKalpha and IKKbeta, necessary for NF-kappaB activation. Cell 1997; 91: 243-252.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Scheidereit C. Signal transduction: docking IKB kinases. Nature 1998; 395: 225-226.[CrossRef][Medline]
[Order article via Infotrieve]
- Ozes ON, Mayo LD, Gustin JA et al. NF-KB activation by tumour necrosis factor requires the Akt serine-threonine kinase. Nature 1999; 401: 82-85.[CrossRef][Medline]
[Order article via Infotrieve]
- Ozes ON, Mayo LD, Gustin JA et al. Reply: kinase regulation in inflammatory response. Nature 2000; 406: 368-368.
- Yamamoto M., Sato S., Hemmi H. et al. Essential role for TIRAP in activation of the signalling cascade shared by TLR2 and TLR4. Nature 2002; 420: 324-329.[CrossRef][Medline]
[Order article via Infotrieve]
- Akira S., Takeda K. Toll-like receptor in innate immunity. Int Immunol 2005; 1: 1-14.[Medline]
[Order article via Infotrieve]
- Glickman MH, Ciechanover A. The ubiquitin-proteasome proteolytic pathway: destruction for the sake of construction. Physiol Rev 2002; 82: 373-428.[Abstract/Free Full Text]
- Ben-Neriah Y. Regulatory functions of ubiquitination in the immune system. Nat Immunol 2002; 3: 20-26.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Lv P., Luo HS, Zhou XP et al. Reversal effect of thalidomide on established hepatic cirrhosis in rats via inhibition of nuclear factor-kappaB/inhibitor of nuclear factor-kappaB pathway. Arch Med Res 2007; 38: 15-27.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Chauhan D., Hideshima T., Mitsiades C. et al. Proteasome inhibitor therapy in multiple myeloma. Mol Cancer Ther 2005; 4: 686-692.[Abstract/Free Full Text]
- Roodman GD Bone building with bortezomib. J Clin Invest 2008; 118: 462-464.[Web of Science][Medline]
[Order article via Infotrieve]
- von Metzler I., Krebbel H., Hecht M. et al. Bortezomib inhibits human osteoclastogenesis. Leukemia 2007; 21: 2025-2034.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Kopp EB, Medzitov R. The Toll-receptor family and control of innate immunity. Curr Opin Immunol 1999; 11: 13-18.[Medline]
[Order article via Infotrieve]
- Dziarski R., Gupta D. Role of MD-2 in TLR2- and TLR4-mediated recognition of Gram-negative and Gram-positive bacteria and activation of chemokine genes. J Endotoxin Res 2000; 6: 401-405.[Medline]
[Order article via Infotrieve]
- Chen CS, Perng WC, Chen CW et al. Thalidomide reduces lipopolysaccharide/zymosan-induced acute lung injury in rats. J Biomed Sci 2004; 11: 591-598.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
- Enomoto N., Takei Y., Hirose M. et al. Protective effect of thalidomide on endotoxin-induced liver injury. Alcohol Clin Exp Res 2003; 27: 2S-6S.[CrossRef][Web of Science][Medline]
[Order article via Infotrieve]
Innate Immunity, Vol. 15, No. 1,
33-41 (2009)
DOI: 10.1177/1753425908099317
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