Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor-alpha production via down-regulation of MyD88 expression Export

@article{citeulike:5960958, abstract = {The effect of thalidomide on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-{alpha} production was studied by using RAW 264.7 murine macrophage-like cells. Thalidomide significantly inhibited LPS-induced TNF-{alpha} production. Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-{alpha} and IKK-{beta} 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-{alpha} 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-{alpha} production. The putative mechanism of thalidomide-induced MyD88 down-regulation is discussed. 10.1177/1753425908099317}, author = {Noman, Abu S. and Koide, Naoki and Hassan, Ferdaus and -E-Khuda and Dagvadorj, Jargalsaikhan and Tumurkhuu, Gantsetseg and Islam, Shamima and Naiki, Yoshikazu and Yoshida, Tomoaki and Yokochi, Takashi}, citeulike-article-id = {5960958}, citeulike-linkout-0 = {http://dx.doi.org/10.1177/1753425908099317}, citeulike-linkout-1 = {http://ini.sagepub.com/content/15/1/33.abstract}, citeulike-linkout-2 = {http://ini.sagepub.com/content/15/1/33.full.pdf}, citeulike-linkout-3 = {http://view.ncbi.nlm.nih.gov/pubmed/19201823}, citeulike-linkout-4 = {http://www.hubmed.org/display.cgi?uids=19201823}, day = {1}, doi = {10.1177/1753425908099317}, journal = {Innate Immunity}, keywords = {nuclear\_factor, p38, signaling, thalidomide, tumor\_necrosis\_factor\_alpha}, month = {February}, number = {1}, pages = {33--41}, posted-at = {2009-10-18 04:49:18}, priority = {2}, title = {Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor-{alpha} production via down-regulation of MyD88 expression}, url = {http://dx.doi.org/10.1177/1753425908099317}, volume = {15}, year = {2009} }

TY - JOUR ID - citeulike:5960958 L3 - citeulike-article-id:5960958 N2 - The effect of thalidomide on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-{alpha} production was studied by using RAW 264.7 murine macrophage-like cells. Thalidomide significantly inhibited LPS-induced TNF-{alpha} production. Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-{alpha} and IKK-{beta} 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-{alpha} 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-{alpha} production. The putative mechanism of thalidomide-induced MyD88 down-regulation is discussed. 10.1177/1753425908099317 IS - 1 JF - Innate Immunity EP - 41 TI - Thalidomide inhibits lipopolysaccharide-induced tumor necrosis factor-{alpha} production via down-regulation of MyD88 expression VL - 15 SP - 33 KW - nuclear_factor KW - p38 KW - signaling KW - thalidomide KW - tumor_necrosis_factor_alpha AU - Noman, Abu AU - Koide, Naoki AU - Hassan, Ferdaus AU - -E-Khuda AU - Dagvadorj, Jargalsaikhan AU - Tumurkhuu, Gantsetseg AU - Islam, Shamima AU - Naiki, Yoshikazu AU - Yoshida, Tomoaki AU - Yokochi, Takashi PY - 2009/02/01/ UR - http://dx.doi.org/10.1177/1753425908099317 ER -