先天性巨结肠症(HSCR)是小儿外科常见病，因其发病机制不明确，导致诊疗的困难。我们前期研究发现细胞外基质fibronectin与neuroligin基因的调控密切相关，证实HSCR的发病机制是“基因异常”和“肠壁微环境变化”共同作用的结果。预实验发现对肠神经系统突触发生、成熟和功能起重要作用的neuroligin基因和炎症因子的表达密切相关，而肠道菌群异常可能是导致炎症环境的诱因之一。于是提出肠道菌群通过影响炎症微环境进而调控neuroligin基因这一假说，并采用免疫组化、PCR、干细胞分离培养、病毒转染、细胞凋亡等技术在人体标本，动物模型和细胞实验三个层面探讨肠道菌群与炎症微环境的关系及对neuroligin基因的影响，为HSCR早期诊断指标的探索及微生物在其治疗中的应用提供理论依据，从新视角揭示HSCR的发病机制，为临床工作提供新思路。

Although Hirschsprung's disease (HSCR) is a common disease in pediatric surgery,it still unable to fully explain the pathogenesis, and therefore leading to the difficulties in diagnosis and treatment. Our prior study found that the revelation of the extracellular matrix fibronectin and neuroligin gene is closely related to the combined results of "gene abnormalities" and " microenvironment changes" theories. Due to the data, we found that inflammatory factors played a key role in the progress of synaptic mature and neuroendocrine function by the regulation of neuroligin gene and are closely related to the intestinal flora abnormalities. So the proposed the theory that intestinal bacteria effected the inflammatory microenvironment to regulate neuroligin gene, which was investigated by the immunohistochemistry, PCR, stem cell isolation, virus transfection and apoptosis in vivo, in vitro and in surgery colon tissues. The results will reveal the relationship between intestinal flora abnormalities and inflammatory microenvironment, and the molecular mechanism in the regulation of neuroligin gene in the pathogenesis of HSCR. We also provide a theoretical basis for the application of early diagnosis of HSCR and the application of microbial mechanisms in HSCR treatment. Changes in the inflammatory environment of the intestinal nervous system provide a new perspective for clinical work.