皮肤是人体最大的器官，是阻止外来病原体进入人体的物理屏障。皮肤表面宿主和共生菌群之间动态的相互调控是维持免疫平衡的重要环节，但目前对菌群-宿主相互作用的理解仍然有限。NLRP3+/R258W功能获得性突变小鼠是研究皮肤炎症和免疫的重要模型。我们的初步研究显示不同的饲养环境使得该突变小鼠的肠道菌群发生变化从而导致皮肤炎症差异，而且初步分析确认了导致这些差异的关键菌种。本研究将在此基础上利用C57BL/6和BALB/C遗传背景的NLRP3+/R258W功能获得性突变小鼠，通过菌群分析、菌株分离、功能重构等一系列实验，探索共生菌群影响皮肤炎症的机理。

Skin is the largest organ of human body, is a physical barrier that prevents pathogenic entrance. There is a delicate balance between the host and the commensal microbiota on the skin surface, which is critical to maitain immune homeostasis and health. However, our understanding about the interaction between host and commensal microbiota is still lacking. The NLRP3+/R258W mouse line is an important model for studying skin inflammation and immunity. Our preliminary data showed that the severity of skin inflammation of NLRP3+/R258W mice was different in novel feeding conditions. Our analysis of the microbiota data also revealed candidate bacterial strains likely contributing to the skin inflammation. In the current project, we will use NLRP3+/R258W mutant mice on either C57BL/6 or BALB/C genetic background to throughly analyze gut-microbiot and skin-microbiota, isolate key bacteria strains and conduct functional studies, aiming to explore the mechanism of microbiota contribution to skin inflammation.