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Toll-like receptor-4 is required for intestinal response to epithelial injury and limiting bacterial translocation in a murine model of acute colitis.
TLDR
DSS treatment of TLR4-/- mice was associated with striking reduction in acute inflammatory cells compared with wild-type mice despite similar degrees of epithelial injury, suggesting that this is the dominant downstream pathway. Expand
Bacterial lipopolysaccharide induces osteoclast formation in RAW 264.7 macrophage cells.
TLDR
LPS-induced osteoclast formation was abolished by anti-tumor necrosis factor (TNF)-alpha antibody, but not antibodies to macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor (NF)-kappaB ligand (RANKL). Expand
Mycobacterium Tuberculosis Heat Shock Proteins Use Diverse Toll-like Receptor Pathways to Activate Pro-inflammatory Signals*
TLDR
It is shown that recombinant, purified, mycobacterial heat shock proteins 65 and 70 induce NF-κB activity in a dose-dependent manner in human endothelial cells and their role in the host immune response to the pathogen may help in the rational design of more effective vaccines or vaccine adjuvants. Expand
Astrocyte elevated gene‐1 (AEG‐1) is induced by lipopolysaccharide as toll‐like receptor 4 (TLR4) ligand and regulates TLR4 signalling
TLDR
Astrocyte elevated gene‐1 was suggested to be a L PS‐responsive gene and involved in LPS‐induced inflammatory response and the prevention of AEG‐1 expression inhibited LPS •induced tumour necrosis factor‐α and prostaglandin E2 production. Expand
Transforming Growth Factor-β Differentially Inhibits MyD88-dependent, but Not TRAM- and TRIF-dependent, Lipopolysaccharide-induced TLR4 Signaling*
TLDR
It is shown that TGF-β1 blocks the NF-κB activation and cytokine release that is stimulated by ligand-induced responses involving the adaptor molecule MyD88 but not the TRAM/TRIF signaling pathway by decreasing MyD 88 protein levels in a dose- and time-dependent manner without altering its mRNA expression. Expand
Differential Roles of Interleukin 15 mRNA Isoforms Generated by Alternative Splicing in Immune Responses in Vivo
TLDR
Two groups of IL-15 Tg mice are constructed to provide information concerning the different roles ofIL-15 isoforms in the immune system in vivo and impaired IFN-γ production upon TCR engagement. Expand
1,25‐Dihydroxyvitamin D3 inhibits lipopolysaccharide‐induced immune activation in human endothelial cells
TLDR
1,25‐(OH)2 D3 pretreatment of human microvessel endothelial cells (HMEC) inhibited the enteric Gram‐negative bacterial lipopolysaccharide (LPS) activation of transcription factor NF‐κB and interleukin (IL)‐6, IL‐8 and regulated upon activation normal T cell exposed and secreted (RANTES) release. Expand
1,25-Dihydroxyvitamin D inhibits lipopolysaccharide-induced immune activation in human endothelial cells.
TLDR
1,25-(OH)2 D3 pretreatment of human microvessel endothelial cells (HMEC) inhibited the enteric gram-negative bacterial lipopolysaccharide (LPS) activation of transcription factor NF-kappaB and interleukin (IL)-6, IL-8 and regulated upon activation normal T cell exposed and secreted (RANTES) release. Expand
TLR/MyD88 and Liver X Receptor α Signaling Pathways Reciprocally Control Chlamydia pneumoniae-Induced Acceleration of Atherosclerosis1
TLDR
It is concluded that C. pneumoniae infection accelerates atherosclerosis in hypercholesterolemic mice predominantly through a TLR/MyD88-dependent mechanism and that LXRα appears to reciprocally modulate and reduce the proatherogenic effects of C.neumoniae infection. Expand
The roles of intrahepatic Vα14+ NK1.1+ T cells for liver injury induced by Salmonella infection in mice
TLDR
It is suggested that αβ T cells bearing NK1.1 and CD4 may be main effector cells for liver injury after Salmonella infection. Expand
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