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Dive into the research topics where Gantsetseg Tumurkhuu is active.

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Featured researches published by Gantsetseg Tumurkhuu.


BMC Cancer | 2006

Intracellular expression of toll-like receptor 4 in neuroblastoma cells and their unresponsiveness to lipopolysaccharide

Ferdaus Hassan; Shamima Islam; Gantsetseg Tumurkhuu; Yoshikazu Naiki; Naoki Koide; Isamu Mori; Tomoaki Yoshida; Takashi Yokochi

BackgroundRecently it has been reported that, toll-like receptors (TLRs) are expressed on a series of tumor cells, such as colon cancer, breast cancer, prostate cancer, melanoma and lung cancer. Although some cancer cells like melanoma cells are known to respond to lipopolysaccharide (LPS) via TLR4, not all cancer cells are positive for TLR4. There is little information on the expression and function of TLR4 in neuroblastoma cells. In this study, we investigated the expression of TLR4 in human neuroblastoma NB-1 cell line.MethodsExpression and localization of TLR4 were detected by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometric analysis, respectively. Activation of nuclear factor (NF)-κB by LPS was detected by degradation of IκB-α and NF-κB luciferase assay. Activation and expression of mitogen-activated protein (MAP) kinase and interferon regulatory factor (IRF)-3 was detected by immunoblot analysis.ResultsHuman NB-1 neuroblastoma cells expressed intracellular form of TLR4, but not the cell surface form. Further, NB-1 cells express CD14, MD2 and MyD88, which are required for LPS response. However, LPS did not significantly induce NF-κB activation in NB-1 cells although it slightly degraded IκB-α. NB-1 cells expressed no IRF-3, which plays a pivotal role on the MyD88-independent pathway of LPS signaling. Collectively, NB-1 cells are capable to avoid their response to LPS.ConclusionAlthough human NB-1 neuroblastoma cells possessed all the molecules required for LPS response, they did not respond to LPS. It might be responsible for intracellular expression of TLR4 or lack of IRF-3.


Laboratory Investigation | 2006

Lethal endotoxic shock using α -galactosylceramide sensitization as a new experimental model of septic shock

Hiroyasu Ito; Naoki Koide; Ferdaus Hassan; Shamima Islam; Gantsetseg Tumurkhuu; Isamu Mori; Tomoaki Yoshida; Shinichi Kakumu; Hisataka Moriwaki; Takashi Yokochi

The effect of α-galactosylceramide (α-GalCer) on lipopolysaccharide (LPS)-mediated lethality was examined. Administration of LPS killed all mice pretreated with α-GalCer, but not untreated control mice. The lethal shock in α-GalCer-sensitized mice was accompanied by severe pulmonary lesions with marked infiltration of inflammatory cells and massive cell death. On the other hand, hepatic lesions were focal and mild. A number of cells in pulmonary and hepatic lesions underwent apoptotic cell death. α-GalCer sensitization was ineffective for the development of the systemic lethal shock in Vα14-positive natural killer T cell-deficient mice. Sensitization with α-GalCer led to the circulation of a high level of interferon (IFN)-γ and further augmented the production of tumor necrosis factor (TNF)-α in response to LPS. The lethal shock was abolished by the administration of anti-IFN-γ or TNF-α antibody. Further, the lethal shock did not occur in TNF-α-deficient mice. Taken together, α-GalCer sensitization rendered mice very susceptible to LPS-mediated lethal shock, and IFN-γ and TNF-α were found to play a critical role in the preparation and execution of the systemic lethal shock, respectively. The LPS-mediated lethal shock using α-GalCer sensitization might be useful for researchers employing experimental models of sepsis and septic shock.


Innate Immunity | 2009

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

Abu Shadat Mohammod Noman; Naoki Koide; Ferdaus Hassan; Imtiaz I.-E-Khuda; Jargalsaikhan Dagvadorj; Gantsetseg Tumurkhuu; Shamima Islam; Yoshikazu Naiki; Tomoaki Yoshida; Takashi Yokochi

The effect of thalidomide on lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production was studied by using RAW 264.7 murine macrophage-like cells. Thalidomide significantly inhibited LPS-induced TNF-α production. Thalidomide prevented the activation of nuclear factor (NF)-KB by down-regulating phosphorylation of inhibitory KB factor (IKB), and IKB kinase (IKK)-α 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-α 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-α production. The putative mechanism of thalidomide-induced MyD88 down-regulation is discussed.


Immunology | 2009

Astrocyte elevated gene‐1 (AEG‐1) is induced by lipopolysaccharide as toll‐like receptor 4 (TLR4) ligand and regulates TLR4 signalling

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

Astrocyte elevated gene‐1 (AEG‐1) is induced by human immunodeficiency virus 1 (HIV‐1) infection and involved in tumour progression, migration and invasion as a nuclear factor‐κB (NF‐κB) ‐dependent gene. The involvement of AEG‐1 on lipopolysaccharide (LPS) ‐induced proinflammatory cytokine production was examined. AEG‐1 was induced via NF‐κB activation in LPS‐stimulated U937 human promonocytic cells. AEG‐1 induced by LPS subsequently regulated NF‐κB activation. The prevention of AEG‐1 expression inhibited LPS‐induced tumour necrosis factor‐α and prostaglandin E2 production. The AEG‐1 activation was not induced by toll‐like receptor ligands other than LPS. Therefore, AEG‐1 was suggested to be a LPS‐responsive gene and involved in LPS‐induced inflammatory response.


Clinical and Experimental Immunology | 2008

The mechanism of development of acute lung injury in lethal endotoxic shock using α-galactosylceramide sensitization

Gantsetseg Tumurkhuu; Naoki Koide; Jargalsaikhan Dagvadorj; Akiko Morikawa; Ferdaus Hassan; Shamima Islam; Yoshikazu Naiki; Isamu Mori; Tomoaki Yoshida; Takashi Yokochi

The mechanism underlying acute lung injury in lethal endotoxic shock induced by administration of lipopolysaccharide (LPS) into α‐galactosylceramide (α‐GalCer)‐sensitized mice was studied. Sensitization with α‐GalCer resulted in the increase of natural killer T (NK T) cells and the production of interferon (IFN)‐γ in the lung. The IFN‐γ that was produced induced expression of adhesion molecules, especially vascular cell adhesion molecule‐1 (VCAM‐1), on vascular endothelial cells in the lung. Anti‐IFN‐γ antibody inhibited significantly the VCAM‐1 expression in α‐GalCer‐sensitized mice. Very late activating antigen‐4‐positive cells, as the counterpart of VCAM‐1, accumulated in the lung. Anti‐VCAM‐1 antibody prevented LPS‐mediated lethal shock in α‐GalCer‐sensitized mice. The administration of LPS into α‐GalCer‐sensitized mice caused local production of excessive proinflammatory mediators, such as tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6 and nitric oxide. LPS caused microvascular leakage of proteins and cells into bronchoalveolar lavage fluid. Taken together, sensitization with α‐GalCer was suggested to induce the expression of VCAM‐1 via IFN‐γ produced by NK T cells and recruit a number of inflammatory cells into the lung. Further, LPS was suggested to lead to the production of excessive proinflammatory mediators, the elevation of pulmonary permeability and cell death. The putative mechanism of acute lung injury in LPS‐mediated lethal shock using α‐GalCer sensitization is discussed.


Innate Immunity | 2008

Hydrogen peroxide induces the production of tumor necrosis factor-α in RAW 264.7 macrophage cells via activation of p38 and stress-activated protein kinase

Noiku Nakao; Tsuyoshi Kurokawa; Toshiaki Nonami; Gantsetseg Tumurkhuu; Naoki Koide; Takashi Yokochi

The effect of hydrogen peroxide (H2O2) on production of tumor necrosis factor (TNF)-α was examined in RAW 264.7 murine macrophage cells. H2O 2 led to production of TNF-α up to 24 h after the treatment, but not nitric oxide in RAW 264.7 cells. H2O2 induced TNF-α production in mouse peritoneal macrophages as well as RAW 264.7 cells. The H2O2induced TNF-α production was prevented by inhibitors of p38 and stress-activated protein kinase (SAPK/JNK), and H2O 2 induced the phosphorylation of p38 and SAPK. Further, H2O 2 significantly augmented the AP-1 activity, but not nuclear factor (NF)-κB activity in RAW 264.7 cells. A high level of intracellular reactive oxygen radicals (ROS) was detected in H2O2-exposed RAW 264.7 cells. Ebselen, a cell permeable antioxidant, prevented the H 2O2-induced TNFα production. H2O2 significantly enhanced lipopolysaccharide (LPS)-induced TNF-α production. Therefore, H 2 O2 was suggested to induce TNF-α production in macrophages via activating p38 and SAPK/JNK as oxidative stress-related signal pathways.


Innate Immunity | 2008

Interleukin-10 inhibits tumor necrosis factor-α production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression

Jargalsaikhan Dagvadorj; Yoshikazu Naiki; Gantsetseg Tumurkhuu; Ferdaus Hassan; Shamima Islam; Naoki Koide; Isamu Mori; Tomoaki Yoshida; Takashi Yokochi

The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, p38 and stress-activated protein kinase (SAPK) in LPS-stimulated RAW 264.7 cells. Although the level of MyD88 protein increased in response to LPS, IL-10 prevented the LPS-induced MyD88 augmentation. There was no significant difference in the MyD88 mRNA expression between the cells pretreated with or without IL-10 in response to LPS. Therefore, IL-10 was suggested to inhibit LPS-induced TNF-α production via reduced MyD88 expression.


Microbiology and Immunology | 2006

Characterization of Biological Activities of Brucella melitensis Lipopolysaccharide

Gantsetseg Tumurkhuu; Naoki Koide; Kazuko Takahashi; Ferdaus Hassan; Shamima Islam; Hiroyasu Ito; Isamu Mori; Tomoaki Yoshida; Takashi Yokochi

Biological activities of lipopolysaccharide (LPS) from Brucella melitensis 16M were characterized in comparison with LPS from Escherichia coli O55. LPS extracted from B. melitensis was smooth type by electrophoretic analysis with silver staining. The endotoxin‐specific Limulus activity of B. melitensis LPS was lower than that of E. coli LPS. There was no significant production of tumor necrosis factor‐α and nitric oxide in RAW 264.7 macrophage cells stimulated with B. melitensis LPS, although E. coli LPS definitely induced their production. On the other hand, B. melitensis LPS exhibited a higher anti‐complement activity than E. coli LPS. B. melitensis LPS as well as E. coli LPS exhibited a strong adjuvant action on antibody response to bovine serum. The characteristic biological activities of B. melitensis are discussed.


Cellular Immunology | 2010

B1 cells produce nitric oxide in response to a series of toll-like receptor ligands

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

The effect of a series of toll-like receptor (TLR) ligands on the production of nitric oxide (NO) in mouse B1 cells was examined by using CD5(+) IgM(+) WEHI 231 cells. The stimulation with a series of TLR ligands, which were Pam3Csk4 for TLR1/2, poly I:C for TLR3, lipopolysaccharide (LPS) for TLR4, imiquimod for TLR7 and CpG DNA for TLR9, resulted in enhanced NO production via augmented expression of an inducible type of NO synthase (iNOS). LPS was most potent for the enhancement of NO production, followed by poly I:C and Pam3Csk4. Imiquimod and CpG DNA led to slight NO production. The LPS-induced NO production was dependent on MyD88-dependent pathway consisting of nuclear factor (NF)-kappaB and a series of mitogen-activated protein kinases (MAPKs). Further, it was also dependent on the MyD88-independent pathway consisting of toll-IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) and interferon regulatory factor (IRF)-3. Physiologic peritoneal B1 cells also produced NO via the iNOS expression in response to LPS. The immunological significance of TLR ligands-induced NO production in B1 cells is discussed.


Microbiology and Immunology | 2008

Receptor activator of nuclear factor-kappa B ligand induces osteoclast formation in RAW 264.7 macrophage cells via augmented production of macrophage–colony-stimulating factor

Shamima Islam; Ferdaus Hassan; Gantsetseg Tumurkhuu; Jargalsaikhan Dagvadorj; Naoki Koide; Yoshikazu Naiki; Tomoaki Yoshida; Takashi Yokochi

RAW 264.7 macrophage cells differentiate into osteoclast‐like cells in the presence of RANKL. Participation of M‐CSF in RANKL‐induced osteoclast formation of RAW 264.7 cells was examined. TRAP‐positive osteoclast‐like cells appeared in RAW 264.7 cells cultured in the presence of RANKL. RANKL‐induced osteoclast formation was markedly inhibited by anti‐M‐CSF antibody. RANKL augmented M‐CSF mRNA expression and M‐CSF production in RAW 264.7 cells. Further, anti‐M‐CSF antibody inhibited the expression of RANK, c‐fms, c‐fos and TRAP mRNA in RANKL‐stimulated RAW 264.7 cells. However, anti‐M‐CSF antibody did not affect the expression of DC‐STAMP in the stimulated cells. Therefore, RANKL was suggested to induce osteoclast formation in RAW 264.7 cells via augmented production of M‐CSF. The putative role of M‐CSF in RANKL‐induced osteoclast formation of RAW 264.7 cells is discussed.

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Naoki Koide

Aichi Medical University

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Ferdaus Hassan

Aichi Medical University

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Shamima Islam

Aichi Medical University

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Isamu Mori

Aichi Medical University

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