表皮葡萄球菌院内感染及耐药与生物膜形成密切相关。前期研究发现双组分信号转导系统SaeRS可调控表皮葡萄球菌生物膜形成能力、自溶和葡萄糖的代谢。表皮葡萄球菌saeRS基因删除突变株生存能力与野生株相比明显降低，自溶率增加，并对青霉素类抗生素敏感性增加。SaeRS正向调控细菌葡萄糖代谢过程，提示葡萄糖在SaeRS介导的表皮葡萄球菌自溶及生物膜形成中起重要作用。本研究拟分析：①葡萄糖代谢是否能影响saeRS突变株的自溶及生存能力；②分析表皮葡萄球菌SaeRS是否通过ccpA-lrg/cid通路调控葡萄糖代谢，从而进一步影响细菌自溶；③新西兰白兔生物膜感染模型验证葡萄糖作用下SaeRS在表皮葡萄球菌自溶形成中起的作用。该研究将有助于阐明葡萄糖影响表皮葡萄球菌自溶形成的机制，并为表皮葡萄球菌感染的治疗提供思路。

Staphylococcus epidermidis is a major cause of nosocomial infections because of biofilm formation. In our previous research, for the first time we found that two-component signal transduction system SaeRS regulated S. epidermidis biofilm formation, autolysis and glucose metabolism. S. epidermidis saeRS gene deletion mutant which was constructed by homologous recombination, showed obvious lower viability, significantly higher Triton X-100 induced autolysis ability and increased susceptibility to penicillin. SaeRS positively regulate glucose metabolism. We postulate that saeRS influence autolysis and biofilm formation by regulating glucose metabolism. The current project proposal plans to analyze further that (1) whether glucose metabolism can influence the autolysis and survival ability of saeRS mutant; (2) whether SaeRS regulate autolysis through ccpA –lrg/cid pathway which plays a centrol role in glucose metabolism; (3) the S. epidermidis saeRS mutant autolysis in animal model in response to glucose. Our findings would shed new lights on the mechanism of S. epidermidis autolysis formation, and provide basis for the therapy of S. epidermidis infection.