scholarly journals miR-16-1 expression, heat shock protein 70 and inflammatory reactions in astrocytes of mice with epilepsy induced by encephalitis B virus infection

2017 ◽  
Vol 14 (1) ◽  
pp. 495-498 ◽  
Author(s):  
Yue Yao ◽  
Yujia Yang ◽  
Xuehua He ◽  
Xia Wang
2012 ◽  
Vol 287 (15) ◽  
pp. 12387-12394 ◽  
Author(s):  
Pawel Stocki ◽  
Xiao N. Wang ◽  
Anne M. Dickinson

Heat shock protein 70 (Hsp70) has gained a lot of attention in the past decade due to its potential immunoregulatory functions. Some of the described proinflammatory functions of Hsp70 became controversial as they were based on recombinant Hsp70 proteins specimens, which were later shown to be endotoxin-contaminated. In this study we used low endotoxin inducible Hsp70 (also known as Hsp72, HSPA1A), and we observed that after a 24-h incubation of monocyte-derived immature dendritic cells (mo-iDCs) with 20 μg/ml of low endotoxin Hsp70, their ability to stimulate allogenic T cells was reduced. Interestingly, low endotoxin Hsp70 also significantly reduced T cell responses when they were simulated with either IL-2 or phytohemagglutinin, therefore showing that Hsp70 could alter T cell responses independently from its effect on mo-iDCs. We also reported a greater response of Hsp70 treatment when activated versus nonactivated T cells were used. This effect of Hsp70 was similar for all tested populations of T cells that included CD3+, CD4+, or CD8+. Taken together, our observations strongly suggest that Hsp70 might dampen, rather than provoke, T cell-mediated inflammatory reactions in many clinical conditions where up-regulation of Hsp70 is observed.


2012 ◽  
Vol 93 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Yong-Zhe Zhu ◽  
Ming-Mei Cao ◽  
Wen-Bo Wang ◽  
Wen Wang ◽  
Hao Ren ◽  
...  

Japanese encephalitis virus (JEV) is an enveloped flavivirus and the most common agent of viral encephalitis. It enters cells through receptor-mediated endocytosis and low pH-triggered membrane fusion. Although lipid rafts, cholesterol-enriched lipid-ordered membrane domains, have been shown to participate in JEV entry, the mechanisms of the early events of JEV infection, including the cellular receptors of JEV, remain largely unknown. In the current study, it was demonstrated that heat-shock protein 70 (HSP70), rather than other members of the HSP70 family, was required for JEV entry into a human cell line. Cell-surface expression of HSP70 and a direct interaction between JEV envelope (E) protein and HSP70 were observed. Biochemical fractionation showed that HSP70 clearly migrated into the raft fraction after virus infection and co-fractioned with E protein. Depletion of cholesterol shifted the E protein and HSP70 to a non-raft membrane and decreased JEV entry without affecting virus binding to host cells. Notably, recruitment of HSP70 into lipid rafts was required for activation of the phosphoinositide 3-kinase/Akt signalling pathway in the early stage of JEV infection. These results indicate that lipid rafts facilitate JEV entry, possibly by providing a convenient platform to concentrate JEV and its receptors on the host-cell membrane.


2001 ◽  
Vol 120 (5) ◽  
pp. A152-A152
Author(s):  
H SUZUKI ◽  
S NAGAHASHI ◽  
M MIYAZAWA ◽  
M MORI ◽  
H NAGATA ◽  
...  

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