p20, Molecular Shortstop for Inflammatory Lung Diseases

描述（申请人摘要）：转录因子CAAT增强子 结合蛋白β（C/EBP β）是一个关键因素， 反应具体地，编码促炎性细胞因子的基因的表达， 细胞因子IL-6和IL-8受C/EBP β调节。C/EBPbeta可以是 取决于主要亚型的炎症激活剂或抑制剂 制作。我们的数据表明，培养的气道上皮细胞 IL-6和IL-8的产生增加抑制性C/EBP β的产生 同种型（p20）和具有过度炎症反应细胞 产生减少的同种型。此外，当动物被给予 内毒素存在抑制性C/EBP β的肺产生减少 同种型和激活剂同种型的产生增加。自从IL-6 产生与人类败血症的严重程度相关， 减少IL-6可以改善这种情况下的结果，我们相信增加IL-6可以改善这种情况下的结果。 肺中抑制性C/EBP β亚型可能是治疗 败血症的肺部并发症

DESCRIPTION (Applicant's abstract): The transcription factor CAAT enhancer binding protein beta (C/EBPbeta) is a key factor orchestrating the inflammatory response. Specifically, expression of the genes encoding the pro-inflammatory cytokines IL-6 and on IL-8 are regulated by C/EBPbeta. C/EBPbeta can be either an activator or an inhibitor of inflammation depending on the dominant isoforms produced. Our data indicate that airway epithelial cells in culture terminate production of IL-6 and IL-8 increasing production of inhibitory C/EBPbeta isoform (p20) and that cells that have an exaggerated inflammatory response produce decreased amounts of this isoform. In addition, when animals are given endotoxin there is a decrease in lung production of the inhibitory C/EBPbeta isoform and an increase in production of the activator isoform. Since IL-6 production correlates with severity of sepsis in humans and interventions that decrease IL-6 improve outcome in that setting, we believe that increasing the inhibitory C/EBPbeta isoform in the lungs could be therapeutic for the pulmonary complications of sepsis.