最新研究表明代谢产物通过调控Treg细胞参与炎症性疾病。我们前期应用代谢组学方法筛选出溶血磷脂酰甘油(LPG)在嗜酸粒细胞性哮喘组外周血高表达；前期动物实验显示LPG引起小鼠急性哮喘模型嗜酸粒细胞炎症、气道IL-10水平降低，且二者相关；前期体外实验显示：在Treg细胞极化条件下，LPG抑制人外周血naive CD4+T细胞增殖及向Treg细胞方向分化。本研究拟通过LPG作用于哮喘小鼠模型、LPG影响人外周血Treg细胞扩增和功能的体外实验，探讨LPG促进哮喘嗜酸粒细胞炎症的机制；并探讨LPG抑制Treg细胞功能的信号通路。证实如下假说：LPG通过减少Treg 细胞数量及抑制其功能，促进Th2炎症反应、促进哮喘嗜酸粒细胞炎症。本项目可为研究哮喘炎症机制提供新的视角（代谢产物可调控免疫反应），有助于阐明LPG在哮喘嗜酸粒细胞炎症的机制，为寻找嗜酸粒细胞性哮喘新的潜在治疗靶点提供思路。

Recent studies have shown that metabolites are involved in inflammatory diseases by regulating Treg cell. In our previous study using metabolomic techniques，we found that lysophosphatidylglycerol (LPG) was highly expressed in the serum of the eosinophilic asthma group. Our previous animal experiments showed that LPG induced eosinophilic inflammation and decreased airway IL-10 levels in mice with acute asthma, and the two were correlated. We also found that LPG inhibits the proliferation of CD4+ naive T cells in human peripheral blood and differentiation of CD4+ naive T cells into Treg cells under Treg cell polarization condition in vitro. The mechanisms of LPG in the eosinophilic inflammation of asthma by regulating Treg cells still remain unclear. This study is to investigate the mechanism of LPG in promoting asthmatic eosinophilic inflammation and signal pathway of inhibiting Treg cells function using mice asthma model and human peripheral blood Treg cells in vitro. We want to confirm the hypothesis that LPG promotes Th2 inflammation and eosinophilic inflammation in asthma by reducing the number of Treg cells and inhibiting their function.This study will provide a new perspective that metabolites can regulate immune response，help to clarify the role of LPG in the inflammatory mechanism of asthma, and provide a new potential therapeutic target for asthma.