众多研究表明巨噬细胞（Mϕ）在哮喘炎症的发生发展过程中发挥重要作用，但Mϕ炎症调控的分子机制却不甚清楚。非编码RNA参与了各种细胞的炎症调控，我们的预实验结果显示LncRNA TRPM2-AS在哮喘儿童的PBMC、LPS以及尘螨提取物活化的THP-1中均表达升高，当敲低TRPM2-AS表达后，Mϕ的炎症因子IL-4、IL-6、IL-10、TNF、IFN-γ、IL-1β等均出现下调；然而TRPM2蛋白mRNA水平却未伴随着TRPM2-AS上调和下调发生变化，但当敲低TRPM2-AS时，TRPM2蛋白水平随之下调，提示TRPM2-AS可能通过影响TRPM2蛋白翻译后稳定性来参与Mϕ的炎症调控。本课题拟在已有预实验基础上进一步探讨TRPM2-AS在Mϕ炎症调控中的主动作用，及调控TRPM2蛋白翻译后稳定的具体机制和工作模式，从而为Mϕ的炎症调控提供新的解释，为哮喘防治提供新的思路。

Accumulating evidence suggests that macrophage play important role in the onset and development of asthma. However, the detail underlying molecular mechanisms of inflammation produced in macrophages is largely unclear. Previous studies reveal that non-coding RNAs are involved in the regulation of inflammation in many types of cells. Our preliminary experiments showed that the exprssions of LncRNA TRPM2-AS were significantly increased in PBMC purified from asthma children, LPS or HDM stimulated THP-1 cells, compared to normal PBMC or untreated THP-1 cells. The expression of some inflammation cytokines including IL-4、IL-6、IL-10、TNF、IFN-γ、IL-1β were obviously decreased in TRPM2-AS down-regulated THP-1 cells than those in WT THP-1 cells while stimulated with LPS. To our surprise, the mRNA level of TRPM2 were not changed anymore neither in TRPM2-AS upregulated THP-1 cells nor in TRPM2-AS down-regulated THP-1 cells. But the protein level of TRPM2 was abruptly decreased in TRPM2-AS down-regulated THP-1 cells. All above preliminary data suggested that TRPM2-AS may regulate the inflammation of macrophage by stabilizing the TRPM2 protein on post-translation level. Thus, in this project, We aim to further explore the active function of TRPM2-AS in macrophage-produced inflammation and detail mechanism of TRPM2-AS in regulating the stabilization of TRPM2 protein, and the working model of TRPM2 in macrophage. We hope this research can initiate a new explanation for the regulation of macrophage inflammation, and give a new suggestion for the treatment of asthma.