Extracellular Hsp70 (eHsp70) can act as damage-associated molecular pattern (DAMP) via Toll-like receptors TLR2 and TLR4, and stimulate immune and inflammatory responses leading to sterile inflammation and propagation of already existing inflammation. It was found elevated in the blood of patients w …

2006年5月29日 · Here we report a novel mechanism of Hsp70 for preventing LPS-induced NF-κB activation in RAW264.7 macrophage-like cells. Our results show that Hsp70 can associate with TRAF6 physically in the TRAF-C domain and prevent TRAF6 ubiquitination. The stimulation of LPS dissociates the binding of Hsp70 and TRAF6 in a time-dependent manner.

2018年5月1日 · In this study, we explored the effects of extracellular Hsp70 when presented alone or together with well-known pathogen-associated molecular pattern (PAMP) molecules, LPS, and LTA, on inflammatory response determined by the levels of secreted pro-inflammatory cytokines (IL-1α, IL-6, IL-8, and TNF-α).

2002年4月26日 · In this report, we address the signal transduction cascade stimulated by exogenous HSP70 and reveal that HSP70-induced NF-κB promoter activity is MyD88-dependEnt, CD14-dependEnt, and is transduced via both TLR2 and TLR4. In addition, we show that TLR2 and TLR4 synergize to greatly augment HSP70-induced cytokine production.

Repression of LPS-induced cytokines expressions by HSP70 upregulation was associated with inhibited IκBα degradation and nuclear factor kappa-B (NF-κB) p65 nuclear translocation in liver, suggesting that HSP70 overexpression may regulate LPS-induced cytokines expression through NF-κB pathway.

Our data demonstrate for the first time that HSP70 overexpression with adenovirus injection prevented the LPS-induced increase in TNF-alpha and IL-6 levels in rats.

实验结果表明SA 预处理组HSP的含量在0.5 h，1.5 h，6 h三个时间点都明显高于LPS组 (P＜0.05)，说明SA预处理可增加HSP70的表达。 在急性肝损伤时，血浆ALT水平的升高在2 h后12 h前[6]，因此本实验选择测定肝损伤后6 h血浆ALT的水平。 结果显示，肝损伤组ALT明显高于对照组及SA预处理组，说明增加HSP70的表达对肝损伤具有保护意义。

2006年5月29日 · Here we report a novel mechanism of Hsp70 for preventing LPS-induced NF-kappaB activation in RAW264.7 macrophage-like cells. Our results show that Hsp70 can associate with TRAF6 physically in the TRAF-C domain and prevent TRAF6 ubiquitination. The stimulation of LPS dissociates the binding of Hsp70 and TRAF6 in a time-dependent manner.

We hypothesised that extracellular heat shock protein 70 (eHsp70), a damage-associated molecular pattern elevated in serum of COPD patients, induces inflammation and alters cigarette smoke and LPS/LTA-induced inflammatory effects in the airway epithelium.

HSP70 treatment improved myocardial tissue damage, survival rate and cardiac dysfunction caused by CLP. Additionally, HSP70 intervention reversed LPS-induced mitochondrial destabilization, inhibited activation of the NLRP3 inflammasome, caspase-1, GSDMD and GSDMD-N, and decreased pyroptosis.