沙门菌鞭毛蛋白活化TLR5和NLRC4通路诱导的炎性应答在机体抗菌感染中发挥重要作用，其调节机制是重要科学问题。LncRNA可在表观遗传、转录及转录后水平调控基因表达，其对免疫应答的调控受到广泛关注。LncRNA对鞭毛蛋白诱导炎性应答的调控鲜有报道。基于此，本研究以小鼠巨噬细胞为模型，通过RNA-seq技术筛选获得了鞭毛蛋白诱导炎性过程中显著上调的lncRNA-Gm26809；拟利用腺病毒过表达或基因沉默系统通过体内外实验评价Gm26809在鞭毛蛋白诱导炎性应答过程中的功能；以TLR5和NLRC4信号通路为切入点，利用RNA pull down、RIP、RNA与蛋白质共定位技术鉴定Gm26809的靶蛋白，初步阐明lncRNA对鞭毛蛋白诱导炎性应答的调控作用，并揭示其作用分子机制，以期为非编码RNA对免疫应答的调控提供新的理论基础，为机体的抗菌感染研究和炎性疾病的治疗提供新的靶点和思路。

Activation of the TLR5 and/or NLRC4 signaling pathways by flagellin and the resulting immune responses play important roles in host anti-bacterial immunity. And the regulation of signaling and the corresponding mechanisms are important topics in immunology. LncRNA can regulate gene expression at epigenetic, transcriptional, and post-transcriptional levels. And the regulation role of lncRNA in the innate immune response have attracted much attention. As far, the regulation of LncRNA on flagellin-induced inflammatory responses has not been reported. Thus, in this project, we identified that the expression level of lncRNA-Gm26809 was up-regulated in flagellin-treated mouse peritoneal macrophages by RNA-seq and qRT-PCR. The adenovirus overexpression or gene silencing system are used to evaluate the function of Gm26809 in inflammatory response induced by flagellin in vitro and in vivo. We will identify target proteins of Gm26809 by RNA pull down, RIP, RNA and protein colocalization techniques based on TLR5 and NLRC4 signaling pathways. The function and molecular mechanism research of Gm26809 in regulation of inflammatory response induced by flagellin will provide a new theoretical basis for the regulation of immune response by non-coding RNA, and provide new target and method for the treatment of bacterial infection and inflammatory diseases.