乳房炎给奶牛养殖业造成巨大的经济损失。目前抗生素仍然是其预防和治疗的主要手段，但是随之带来的细菌耐药性及食品抗生素残留等问题日趋严重。因此，迫切需要寻找安全、有效的防治乳房炎的方法。GPR109A是Gi蛋白偶联的受体。本课题组前期发现在奶牛和小鼠乳腺上皮细胞中均有GPR109A表达，并且其可能具有调节LPS诱导的乳腺上皮细胞炎症反应的功能。但是GPR109A能否抑制LPS诱导的乳腺上皮细胞炎症反应，迄今国内外尚无报道。因此，本项目拟应用体外乳腺上皮细胞炎症模型及在体GPR109A敲除小鼠乳房炎模型，利用Western blotting、荧光定量PCR、免疫荧光、ELISA、EMSA等技术，从分子、细胞和整体水平探讨GPR109A对LPS诱导的乳腺上皮细胞炎症反应的影响及其分子机制，揭示GPR109A在乳房炎发生发展中的作用，以期为乳房炎的防治提供新的靶点。

Mastitis causes the greatest economic loss to dairy farming around the world. Currently, the treatment of mastitis mainly depends on antibiotic. However, it may lead to drug resistant bacteria and also antibiotic residue in the human food chain. Therefore, looking for a novel alternative therapy for bovine mastitis is an urgent topic. G protein coupled receptor109A (GPR109A) is a seven-transmembrane G-protein-coupled receptor of the Gi family. In previous study, we found that GPR109A is expressed in mammary epithelial cells from dairy cow and mice, and it may regulate LPS-induced inflammation in mammary epithelial cells. However, little is known about whether GPR109A could inhibit LPS-induced inflammation in mammary epithelial cells. Therefore, we attempt to clarify regulatory mechanisms of GPR109A on LPS-induced inflammation in mammary epithelial cells as well as its potential roles in development of mastitis, using LPS-induced inflammation in mammary epithelial cells from dairy cow and WT/ GPR109A knockout mice, LPS-induced mastitis in GPR109A knockout mice and technology such as Western blotting, Realtime-PCR, immunofluorescence, ELISA, EMSA and so on. Our finding will provide a new target for the prevention and treatment of mastitis.