基于乳房链球菌感染能引起胞浆Ca2+浓度升高，Ca2+浓度升高介导的炎性反应与肌醇磷脂系统及核转录因子NFAT、NF-κB有密切的联系，NFAT激活对炎症的调控有促炎及抗炎两方面，而牛磺酸跨膜转运会引起胞浆Ca2+浓度降低，我们提出肌醇磷脂-Ca2+-NFAT途径在牛磺酸缓解乳房链球菌感染的过程中有重要作用的假设。为此，研究拟将牛磺酸、乳房链球菌与各种乳腺功能细胞按一定顺序、组合共孵育，适时用针对Ca2+动员及NFAT、NF-κB转录激活的特异性拮抗剂阻断/抑制相关信号通路，通过比较不同处理间肌醇磷脂系统组分、Ca2+浓度、转录因子活性及其下游效应分子、胞内菌数及细胞损伤的差异，首先从细胞水平阐明肌醇磷脂-Ca2+-NFAT途径在牛磺酸缓解乳房链球菌感染中的作用，然后在山羊模型上进行整体验证。研究的开展有助于阐明营养元素牛磺酸的抗感染机理，为乳腺炎的防控提供新的思路。

Streptococcus uberis (S. uberis) infection upregulates cytoplasmic Ca2+ concentration. Inflammation mediated by Ca2+ need the participation of phosphoinositide system and transcription factors NFAT and NF-κB. Activated NFAT controls inflammation by its pro- and anti- inflammatory properties and membrane transport of taurine resulting in a reduction of cytoplasm Ca2+ concentration. We hypothesize that the phosphoinositide-Ca2+-NFAT pathway plays a critical role in attenuating taurine-associated S. uberis infection. To test this hypothesis we will co-culture taurine and S. uberis with different mammary target cells in a variety of permutations and combinations. A variety of Ca2+ mobilization inhibitors and NFAT, NF-κB transcription activators will be used to inhibit the relevent signaling pathways. The phosphoinositide component, Ca2+ concentration, transcription factors activity, downstream effectors, the number of intracellular bacteria and cell injury will be quantified. Then, these will be carried out in a goat model. This research will help elucidate the cellular mechanism of phosphoinositide-Ca2+-NFAT signaling in the taurine amelioration of S. uberis infection. This study will help to delineate the anti-inflammatory mechanism of nutritional taurine and provide insight into dietary methods for the prevention and control of mastitis.