scholarly journals Sodium Methyldithiocarbamate Inhibits MAP Kinase Activation through Toll-like Receptor 4, Alters Cytokine Production by Mouse Peritoneal Macrophages, and Suppresses Innate Immunity

2005 ◽  
Vol 87 (1) ◽  
pp. 75-85 ◽  
Author(s):  
Stephen B. Pruett ◽  
Qiang Zheng ◽  
Carlton Schwab ◽  
Ruping Fan
Keyword(s):  
Innate Immunity ◽  
Map Kinase ◽  
Cytokine Production ◽  
Peritoneal Macrophages ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Kinase Activation ◽  
Sodium Methyldithiocarbamate ◽  
Mouse Peritoneal Macrophages

scholarly journals Bacteroides fragilis-Derived Lipopolysaccharide Produces Cell Activation and Lethal Toxicity via Toll-Like Receptor 4

2005 ◽  
Vol 73 (9) ◽  
pp. 5620-5627 ◽  
Author(s):  
Giuseppe Mancuso ◽  
Angelina Midiri ◽  
Carmelo Biondo ◽  
Concetta Beninati ◽  
Maria Gambuzza ◽  
...  
Keyword(s):  
Cell Activation ◽  
Cytokine Production ◽  
Biological Activities ◽  
Endotoxic Shock ◽  
Intestinal Flora ◽  
Bacteroides Fragilis ◽  
Peritoneal Macrophages ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
In Cells

ABSTRACT Bacteroides fragilis, which is part of the normal intestinal flora, is a frequent cause of serious disease, especially in diabetic and surgical patients. In these conditions, B. fragilis lipopolysaccharide (LPS) is likely to play a major pathophysiologic role. B. fragilis LPS is structurally different from classical enterobacterial LPS, whose biological activities are mediated by Toll-like receptor 4 (TLR4) activation. The ability of B. fragilis LPS to activate TLR4 and TLR2 was investigated here, since evidence on this issue is scarce and controversial. Each of four different protein-free B. fragilis LPS preparations could induce interleukin-8 responses in cells cotransfected with TLR4/CD14/MD2 but not TLR4/CD14 alone. Two of the preparations also induced cytokine production in cells cotransfected with TLR2/CD14 or in peritoneal macrophages from TLR4 mutant C3H/HeJ mice. Both of these activities, however, were lost after repurification with a modified phenol reextraction procedure. Importantly, all preparations could induce endotoxic shock in TLR2-deficient mice, but not in TLR4 mutant C3H/HeJ mice. Consistent with these findings, anti-TLR4 and anti-CD14, but not anti-TLR2, antibodies could inhibit B. fragilis LPS-induced cytokine production in human monocytes. Collectively, these results indicate that B. fragilis LPS signals via a TLR4/CD14/MD2-dependent pathway, and it is unable to activate TLR2. Moreover, our data document the occurrence of TLR2-activating contaminants even in highly purified B. fragilis LPS preparations. This may explain earlier contradictory findings on the ability of B. fragilis LPS to activate cells in the absence of functional TLR4. These data may be useful to devise strategies to prevent the pathophysiologic changes observed during B. fragilis sepsis and to better understand structure-activity relationships of LPS.

scholarly journals The contribution of miR-122 to the innate immunity by regulating toll-like receptor 4 in hepatoma cells

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Liyu Shi ◽  
Xiaoqiu Zheng ◽  
Yuzhuo Fan ◽  
Xiaolan Yang ◽  
Aimei Li ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Hepatoma Cells ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Toll-like receptor 4 ablation in mdx mice reveals innate immunity as a therapeutic target in Duchenne muscular dystrophy

2014 ◽  
Vol 24 (8) ◽  
pp. 2147-2162 ◽  
Author(s):  
Christian Giordano ◽  
Kamalika Mojumdar ◽  
Feng Liang ◽  
Christian Lemaire ◽  
Tong Li ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Duchenne Muscular Dystrophy ◽  
Muscular Dystrophy ◽  
Therapeutic Target ◽  
Mdx Mice ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4
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