COPD是吸烟造成损伤相关分子模式（DAMPs）激活模式识别受体启动的慢性炎症，促炎介质LTB4与受体BLT1结合可影响模式识别受体、MyD88等表达促进核转录因子NF-ｋB激活导致炎症级联放大；SOCS1是内源性负反馈调节分子，通过调节JAK/STAT1/MyD88通路抑制固有免疫介导的炎症。我们发现COPD患者肺泡巨噬细胞及肺组织中SOCS1表达远低于非COPD组，且与LTB4存在显著负相关；因此推测：COPD持续炎症反应与SOCS1负调控不足及LTB4通路激活有关，目前国内外对此领域缺乏研究。本课题拟从：1）COPD患者LTB4与SOCS1表达及相关性研究,探讨SOCS1/ LTB4/BLT1在早期炎症启动中的作用；2）通过BLT1基因敲除小鼠、SOCS1慢病毒过表达小鼠模型，探究调节SOCS1/LTB4/BLT1通路抑制固有免疫反应强度的可行性，以期提供COPD早期有效抗炎治疗。

COPD is a chronic inflammatory disease related to tobacco smoke,which induces danger- associated molecular patterns (DAMPs) and regulates pattern-recognition receptor.Leukotriene B4(LTB4) ,the most important pro-inflammatory mediators and its BLT1 receptors mediated the pattern-recognition receptors ,MyD88 ,which leads to the inflammatory amplification by promoting the activation of nuclear transcription factor NF-ｋB. SOCS1,the endogenous negative-feedback regulator,suppresses the inappropriate inflammation by regulating JAK/STAT1/MyD88 passway.Our study have observed that SOCS1 expression levels in COPD patients decreased dramatically compared with non-COPD group in alveolar macrophages and lung tissues, the expression of SOCS1 were negatively correlated with LTB4.We hypothesized that lack of SOCS1 and LTB4/BLT1 activation enhances persistent inflammation in COPD.However the role of SOCS1/LTB4/BLT1 signaling pathway is unclear .In this study,we will investigate 1)The expression of SOCS1 , LTB4 and their correlation in COPD patients, to explore the role of SOCS1/LTB4/BLT1 signaling in early initiated inflammation.2）Regulating SOCS1/LTB4/BLT1 signaling is expected to decrease the intensity of innate immunity in COPD，by the model of BLT1 gene knockout mice and SOCS1 – overexpression lentiviral vector in mice.Perhaps it may lead to more effective therapies in the treatment of early inflammation of COPD.