单核细胞TH1细胞因子表达能力受抑与抗原提呈能力降低是脓毒症免疫麻痹的重要病理机制，但治疗药物缺乏。我们发现钠钾ATP酶配体哇巴因能恢复单核细胞TH1细胞因子表达能力，逆转脓毒症内毒素耐受，提高存活率，其机制在于哇巴因能刺激RNA 结合蛋白HuR出核，HuR转录后稳定TNFα、GM-CSF、IFN-γ mRNA，从而对TH1细胞因子表达重新编程。进一步研究发现HuR 胞浆内积聚与哇巴因诱导的lincRNA152表达相关，lincRNA152与HuR形成复合物。由此推测在脓毒症免疫抑制状态下，通过激活单核细胞lincRNA152表达，形成lincRNA152/HuR复合物将HuR滞留于胞浆中，并“锚定”HuR在TH1细胞因子mRNA 的3’非翻译区，可以稳定TH1细胞因子mRNA，增强机体清除病原微生物能力。研究lincRNA152/HuR精密调控细胞因子稳定性为脓毒症诊疗提供新的理论依据。

Impairment of TH1 cytokine-producing and antigen-presenting ability of monocytes is important contributing factors for sepsis-induced immunoparalysis. In our previous investigation, we found ouabain, as a specific Na+,K+-ATPase ligand, was able to restore the impaired TNF-α-producing activity in human monocytes, reverse immunoparalysis and improve survival, the underlying mechanism was that ouabain stimulated HuR nuclear export, which posttranscriptionally stabilized TNF-α, GM-CSF and IFN-γmRNA stability, and thereby reprogramming TH1 cytokine expression. Further analysis revealed that cytoplasm accumulation of HuR was relevant to ouabain-induced lincRNA152 production, lincRNA152 forms a complex with HuR. Taken these facts together, we presume that lincRNA152 plays an important role in the pathogenesis of sepsis-induced immunoparalysis. By interacting with HuR, lincRNA152 will prevent the re-entry of HuR into nucleus,fix the HuR onto the 3’-UTR of TH1 cytokines mRNA, and strengthen the effect of HuR on TH1 cytokines mRNA stabilization, finally increasing host immunity against invading microorganism. Investigation on the upregulation of lincRNA152 and interplays between lincRNA152 and HuR as well as the underlying mechanism provides novel insight into the pathological mechanism for sepsis.