scholarly journals Dicalcium Silicate Induced Proinflammatory Responses through TLR2-Mediated NF-κB and JNK Pathways in the Murine RAW 264.7 Macrophage Cell Line

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Shixiang Lai ◽  
Liangjiao Chen ◽  
Wei Cao ◽  
Shiman Cui ◽  
Xingyang Li ◽  
...  

Proinflammatory responses are important aspects of the immune response to biomaterials, which may cause peri-implantitis and implant shedding. The purpose of this study was to test the cytotoxicity and proinflammatory effects of dicalcium silicate particles on RAW 264.7 macrophages and to investigate the proinflammatory response mechanism induced by C2S and tricalcium phosphate (TCP). C2S and TCP particles were characterized using scanning electron microscopy (SEM), energy spectrum analysis (EDS) and X-ray diffraction (XRD). Cytotoxicity and apoptosis assays with C2S and TCP in the murine RAW 264.7 cell line were tested using the cell counting kit-8 (CCK-8) assay and flow cytometry (FCM). The detection results showed that C2S and TCP particles had no obvious toxicity in RAW 264.7 cells and did not cause obvious apoptosis, although they both caused an oxidative stress response by producing ROS when the concentrations were at 100 μg/mL. C2S particles are likely to induce a proinflammatory response by inducing high TLR2, TNF-α mRNA, TNF-α proinflammatory cytokine, p-IκB, and p-JNK1 + JNK2 + JNK3 expression levels. When we added siRNA-TLR2-1, a significant reduction was observed. These findings support the theory that C2S particles induce proinflammatory responses through the TLR2-mediated NF-κB and JNK pathways in the murine RAW 264.7 macrophage cell line.

2012 ◽  
Vol 41 (11) ◽  
pp. 1521-1527 ◽  
Author(s):  
A-Reum Yu ◽  
Ho-Young Park ◽  
In-Wook Choi ◽  
Yong-Kon Park ◽  
Hee-Do Hong ◽  
...  

Author(s):  
Rosa Ana Sueiro-Benavides ◽  
Jose Manuel Leiro-Vidal ◽  
Aarón Ángel Salas-Sánchez ◽  
J. Antonio Rodríguez-González ◽  
Francisco J. Ares-Pena ◽  
...  

2001 ◽  
Vol 69 (5) ◽  
pp. 3214-3223 ◽  
Author(s):  
Xiaohan Du ◽  
Martin G. Low

ABSTRACT Serum glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) activity is reduced over 75% in systemic inflammatory response syndrome. To investigate the mechanism of this response, expression of the GPI-PLD gene was studied in the mouse monocyte-macrophage cell line RAW 264.7 stimulated with lipopolysaccharide (LPS; 0.5 to 50 ng/ml). GPI-PLD mRNA was reduced approximately 60% in a time- and dose-dependent manner. Oxidative stress induced by 0.5 mM H2O2 or 50 μM menadione also caused a greater than 50% reduction in GPI-PLD mRNA. The antioxidant N-acetyl-l-cysteine attenuated the down-regulatory effect of H2O2but not of LPS. Cotreatment of the cells with actinomycin D inhibited down-regulation induced by either LPS or H2O2. The half-life of GPI-PLD mRNA was not affected by LPS, or decreased slightly with H2O2, indicating that the reduction in GPI-PLD mRNA is due primarily to transcriptional regulation. Stimulation with tumor necrosis factor alpha (TNF-α) resulted in ∼40% reduction in GPI-PLD mRNA in human A549 alveolar carcinoma cells but not RAW 264.7 cells, suggesting that alternative pathways could exist in different cell types for down-regulating GPI-PLD expression during an inflammatory response and the TNF-α autocrine signaling mechanism alone is not sufficient to recapitulate the LPS-induced reduction of GPI-PLD in macrophages. Sublines of RAW 264.7 cells with reduced GPI-PLD expression exhibited increased cell sensitivity to LPS stimulation and membrane-anchored CD14 expression on the cell surface. Our data suggest that down-regulation of GPI-PLD could play an important role in the control of proinflammatory responses.


2008 ◽  
Vol 229 (2) ◽  
pp. 146-160 ◽  
Author(s):  
Pasi I. Jalava ◽  
Raimo O. Salonen ◽  
Arto S. Pennanen ◽  
Mikko S. Happo ◽  
Piia Penttinen ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Alejandro Escobar ◽  
Enzo Candia ◽  
Sebastian Reyes-Cerpa ◽  
Bélgica Villegas-Valdes ◽  
Tanya Neira ◽  
...  

Neisseria gonorrhoeaeis the etiological agent of gonorrhoea, which is a sexually transmitted disease widespread throughout the world.N. gonorrhoeaedoes not improve immune response in patients with reinfection, suggesting that gonococcus displays several mechanisms to evade immune response and survive in the host.N. gonorrhoeaeis able to suppress the protective immune response at different levels, such as B and T lymphocytes and dendritic cells. In this study, we determined whetherN. gonorrhoeaedirectly conditions the phenotype of RAW 264.7 murine macrophage cell line and its response. We established that gonococcus was effectively phagocytosed by the RAW 264.7 cells and upregulates production of immunoregulatory cytokines (IL-10 and TGF-β1) but not the production of proinflammatory cytokine TNF-α, indicating that gonococcus induces a shift towards anti-inflammatory cytokine production. Moreover,N. gonorrhoeaedid not induce significant upregulation of costimulatory CD86 and MHC class II molecules. We also showed thatN. gonorrhoeaeinfected macrophage cell line fails to elicit proliferative CD4+ response. This implies that macrophage that can phagocytose gonococcus do not display proper antigen-presenting functions. These results indicate thatN. gonorrhoeaeinduces a tolerogenic phenotype in antigen-presenting cells, which seems to be one of the mechanisms to induce evasion of immune response.


2012 ◽  
Vol 6 (6) ◽  
pp. 1343-1350 ◽  
Author(s):  
YING LIU ◽  
WEI-WEI SU ◽  
SHENG WANG ◽  
PEI-BO LI

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Ho-young Park ◽  
Heedon Choi ◽  
Areum Yu ◽  
Inwook Choi ◽  
Yoonsook Kim

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