肠道上皮细胞作为内外环境信号转导枢纽，率先识别肠道微生物，释放炎性介质启动天然免疫和适应性免疫。miRNA已被证实广泛调控粘膜免疫，然而，其对肠道上皮细胞炎症反应的调控机制尚不清晰。申请人前期证实，miRNA-novel-272在牙鲆肠道组织和肠道上皮细胞炎症反应初期显著下调，并可以靶向结合促炎基因半乳糖凝集素3（galectin3）。据此提出：miRNA-novel-272通过靶向结合galectin3调控上皮细胞炎症反应。本项目拟进一步开展以下研究：1）明确miRNA-novel-272调控上皮细胞炎症活性；2）解析miRNA-novel-272通过galectin3调控上皮细胞炎症活性；3）探讨galectin3下游炎症信号通路。本项目的实施将揭示miRNA-novel-272对牙鲆肠道上皮细胞炎症反应的调控机制，深化对鱼类肠道炎症反应的认识，为鱼类肠道炎症疾病防控提供科学依据。

As the signal transduction hub of internal and external environment, intestinal epithelial cells take the lead in recognizing intestinal microorganisms and releasing inflammatory mediators that activate natural and adaptive immunity. It has been identified that miRNA regulate the mucosal immunity. However, the mechanism of miRNA on the inflammatory response of intestinal epithelial cells is still not clear. We found that miRNA-novel-272, which could target the proinflammatory gene of galectin3, was significantly down-regulated during the early stage of inflammation in the intestinal tissues and epithelial cells of Paralichthys olivaceus. It is suggested that miRNA-novel-272 may further affect the inflammatory response of epithelial cells by regulating expression of galectin3. This project intends to further carry out the following researches: 1) clarify the regulation role of miRNA-level-272 on epithelial inflammatory activity; 2) make it clear that the regulation of miRNA-level-272 on epithelial inflammatory activity was mediated by galectin3; 3) explore the downstream inflammatory signaling pathway of galectin3. The implementation of this project will reveal the regulatory mechanism of miRNA-novel-272 on the inflammatory response of the intestinal epithelial cells in flounder, deepen the understanding of the fish intestinal inflammatory response, and provide scientific basis for the prevention and control of fish intestinal inflammatory diseases.