scholarly journals IL-33 Enhances Lipopolysaccharide-Induced Inflammatory Cytokine Production from Mouse Macrophages by Regulating Lipopolysaccharide Receptor Complex

2009 ◽  
Vol 183 (2) ◽  
pp. 1446-1455 ◽  
Author(s):  
Quentin Espinassous ◽  
Elvira Garcia-de-Paco ◽  
Ignacio Garcia-Verdugo ◽  
Monique Synguelakis ◽  
Sonja von Aulock ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Receptor Complex ◽  
Inflammatory Cytokine Production ◽  
Mouse Macrophages ◽  
Lipopolysaccharide Receptor

Role of Brd4 in the production of inflammatory cytokines in mouse macrophages treated with titanium particles

2019 ◽  
Vol 97 (11) ◽  
pp. 1028-1034 ◽  
Author(s):  
Yuanzhong Ren ◽  
Yongtao Zhang ◽  
Ze Wang ◽  
Changyao Wang ◽  
Haining Zhang ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Wear Particle ◽  
Raw264.7 Cells ◽  
Inflammatory Cytokine Production ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Ti Particles

Brd4 protein is an important epigenetic regulator involved in the process of inflammatory cytokine production in many diseases. However, whether and how Brd4 participates in the process of wear-particle-induced inflammation remain unclear. This study aimed to investigate the potential role of Brd4 in titanium (Ti) particle-induced inflammatory cytokine production in mouse macrophage RAW264.7 cells. Our experiment detected Brd4 expressed in both normal synovium and periprosthetic osteolysis interface membrane, but the expression increased in the interface membrane as compared with that in normal synovium. Treatment with Ti particles significantly increased TNF-α, IL-6, and IL-1β production in RAW264.7 cells, which was inhibited by JQ1 or Brd4-siRNA. Ti particles enhanced the expression of Brd4, which was abrogated by JQ1. Ti particles enhanced NF-κB p65 and IKK phosphorylation and attenuated IκBα protein expression, which were abrogated by JQ1. Co-immunoprecipitation analysis indicated that Ti particles promoted the binding of Brd4 to acetylated NF-κB p65 (lysine-310), which was also abrogated in JQ1-treated RAW264.7 cells. In conclusion, Brd4 expression increases in interface membrane and Brd4 participates in the production of pro-inflammatory cytokines induced by Ti particles via promoting the activation of NF-κB signaling and binding to acetylated NF-κB p65 (lysine-310) in mouse macrophages.

scholarly journals Neutral Polysaccharide from the Leaves of Pseuderanthemum carruthersii: Presence of 3-O-Methyl Galactose and Anti-Inflammatory Activity in LPS-Stimulated RAW 264.7 Cells

Polymers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1219 ◽  
Author(s):  
Vo Hoai Bac ◽  
Berit Smestad Paulsen ◽  
Le Van Truong ◽  
Andreas Koschella ◽  
Tat Cuong Trinh ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Water Extract ◽  
Mapk Signaling ◽  
Raw 264.7 Cells ◽  
Oxygen Species ◽  
Inflammatory Cytokine Production ◽  
Mouse Macrophages ◽  
Chemotaxonomic Marker

Pseuderanthemum carruthersii (Seem.) Guillaumin is a native tree in Vietnam. The water extract of the leaves from this tree gives a highly viscous product that has been used to heal wounds and treat inflammations. Our previous studies showed that the leaves of P. carruthersii have a high content of polysaccharides. In this study, the structure and influence of the neutral polysaccharide from Pseuderanthemum carruthersii (PCA1) on lipopolysaccharide (LPS)-stimulated RAW264.7 cells were investigated. The PCA1 isolated from P. carruthersii is a galactan-type polysaccharide, containing galactose (77.0%), 3-O-methyl galactose (20.0%), and arabinose (3.0%). Linkage analysis of PCA1 showed that both the 3-O-methyl galactose and galactose were 1,4-linked. The presence of 3-O-methyl galactose units as part of the polysaccharide is important and can be used as a chemotaxonomic marker. The molecular weight of the PCA1 was 170 kDa. A PCA1 concentration of 30–40 μg/mL strongly inhibited TNFα, IL-1β, and IL-6 inflammatory cytokine production, and reactive oxygen species (ROS) release. PCA1 had inhibitory activities on pro-inflammatory cytokine and ROS release in LPS-stimulated mouse macrophages in vitro through MAPK signaling.

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