支气管肺发育不良（BPD）是极低出生体重儿常见的慢性肺部疾病，病死率高，预后差，严重影响了早产儿的生存质量。脂多糖（LPS）是革兰氏阴性细菌细胞壁的主要成分，与多种急慢性肺部疾病的易感性相关，并可在孕鼠中模拟宫内感染的作用。在BPD发生中，宫内感染发挥了关键作用。已有研究表明LPS可通过TLRs信号途径起炎性作用，而SIGIRR则可能对LPS通过多种路径起抑制作用，但目前SIGIRR在宫内感染所致的慢性肺部疾病中的作用尚无报道。本项目在前期研究的基础上拟采用质粒转染、免疫荧光、定量PCR、免疫印迹等方法进一步探讨SIGIRR在调控LPS诱导的BPD中的作用机制，为早期有效防治宫内感染所致的肺损伤奠定理论基础，并为BPD的研究提供新靶点。

Bronchopulmonary dysplasia (BPD) is one of the most common chronic respiratory diseases in very-low-birth-weight infants and characterized with high fatality and poor prognosis, also it influences the quality life in premature infants greatly. Lipopolysaccharide (LPS) is the major part of cell component in Gram-negative bacteria, and related to a variety of acute and chronic diseases. In addition, LPS can simulate the role of intrauterine infection in pregnant mouse. The intrauterine infection plays a pivotal role in the development of BPD. Some studies have shown that inflammation could play a role in LPS signaling pathway via TLRs; meanwhile SIGIRR may also play a part in some LPS induced diseases, but its role in intrauterine infection that leads to premature chronic lung diseases has not been yet reported. This project on the basis of preliminary studies uses the methods of plasmid transfection, immunofluorescence, quantitative PCR, immunoblotting (western blot) and so on to explore the mechanism of SIGIRR in the regulation of LPS-induced BPD for early and effective prevention and treatment which may also provide a new target for the study of BPD.