This study was designed to investigate the role of Pellino1 in lung injury model of sepsis and its anti-inflammation mechanism. C57BL/6 male mice (6–7 weeks old) and Pellino1−/− male mice were subjected to laparotomy followed by extracorporeal cecum mobilization and ligation. THP-1 cells were treated with 500 ng/ml of LPS for 4 h. Both mRNA and protein expression of Pellino1 was increased at time dependence in lung tissue of lung injury model of sepsis mice. Knockout of Pellino1 attenuated lung injury and inhibited inflammation of sepsis mice. While Pellino1 protein enhanced lung injury and increased inflammation of sepsis mice. Pellino1 promoted inflammation in in vitro model of lung injury by TRAF6/ NF-κB signal pathway. TRAF6 inhibitor attenuated the effects of Pellino1 on inflammation and lung injury in mice of sepsis. Similarly, NF-κB inhibitor also suppressed the effects of Pellino1 on inflammation and lung injury in mice of sepsis. The activation of TRAF6 or induction of NF-κB attenuated the effects of Pellino1 on inflammation in in vitro model of sepsis. The inhibition of TRAF6 or suppression of NF-κB reduced the effects of Pellino1 on inflammation in in vitro model of sepsis. These results suggested that Pellino1 promoted inflammation in lung injury model of sepsis by TRAF6/ NF-κB signal pathway.

中文翻译：

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Pellino1通过TRAF6 /NF-κB信号通路促进脓毒症肺损伤模型的炎症

本研究旨在探讨Pellino1在脓毒症肺损伤模型中的作用及其抗炎机制。对C57BL / 6雄性小鼠（6-7周龄）和Pellino1-/-雄性小鼠进行剖腹手术，然后进行盲肠动员和结扎。用500 ng / ml的LPS处理THP-1细胞4小时。在脓毒症小鼠肺损伤模型的肺组织中，Pellino1的mRNA和蛋白表达均随时间增加而增加。敲除Pellino1可减轻肺损伤，并抑制败血症小鼠的炎症。而Pellino1蛋白可增强肺损伤并增加败血症小鼠的炎症。Pellino1通过TRAF6 /NF-κB信号通路促进肺损伤体外模型的炎症。TRAF6抑制剂减弱了Pellino1对败血症小鼠炎症和肺损伤的作用。相似地，NF-κB抑制剂还抑制了Pellino1对脓毒症小鼠炎症和肺损伤的作用。在脓毒症的体外模型中，TRAF6的激活或NF-κB的诱导减弱了Pellino1对炎症的作用。在脓毒症的体外模型中，TRAF6的抑制或NF-κB的抑制降低了Pellino1对炎症的影响。这些结果表明Pellino1通过TRAF6 /NF-κB信号通路促进脓毒症肺损伤模型的炎症。