IgA肾病(IgAN)发病率存在明显种族与地域差异，研究发现新疆慢性牙周炎患者IgAN发病率显著高于非牙周炎，维吾尔人群牙周炎及IgAN患病率均高于当地人群，我们动物实验也观察到牙周炎可促进IgAN病变进展，与牙周炎引发机体炎性反应有关。因此我们提出假说：牙周炎通过激活TLRs信号通路，刺激宿主细胞释放炎症因子，进而引起免疫炎症反应，促进IgAN发生进展。为验证这一假说，我们拟采用高通量测序技术分析维吾尔人群口腔微生物多样性，筛选优势菌群，并据此建立大鼠慢性牙周炎及IgAN模型，检测炎症因子蛋白表达水平及TLR4/9受体水平；分离培养大鼠系膜细胞，阻断细胞TLR4/9信号通路，检测调控前后系膜细胞炎症因子表达及信号通路mRNA水平，明确慢性牙周炎与IgAN的相关性及作用机制。本研究将为新疆维吾尔IgAN患者牙周早期干预治疗奠定理论基础，同时也将为IgAN粘膜致病菌学说提供新的依据。

IgA nephropathy (IgAN) has obvious racial and regional differences of incidence. The study found that, the incidence of IgAN in Xinjiang periodontitis patient was significantly higher than that in non periodontitis, the prevalence rate of periodontitis and the incidence of IgAN were significantly higher in Uygur populations than the local populations.We also observed from the zoopery that, periodontitis can promote the progression of the IgAN, And periodontitis leads to inflammatory reaction. Therefore we put forward a hypothesis that: periodontitis stimulates the host cells to release inflammatory factors through the activation of TLRs signal pathway, and then causes the immune inflammatory reaction, to promote the progression of IgAN. In order to verify this hypothesis, we intend to use high-throughput sequencing technologies to analysis the diversity of oral microorganisms in Uighur populations, screening of dominant bacteries, on the basis of this, to establish chronic periodontitis and IgAN model of a rat, examined the protein expression level of inflammatory factors and the levels of the TLR4/9 receptors; Isolated and cultured rat mesangial cell, blocking the cell's TLR4/9 signaling pathway, to detect the inflammatory factor’s expressions in mesangial cells and the level of mRNA signaling pathway at the before and after of the regulation, to clear the correlations and mechanisms of the chronic periodontitis and IgAN. This study will lay the theoretical foundation for IgAN patients in Xinjiang Uygur populations with early intervention of periodontal treatment, at the same time will also provide new evidences for the IgAN Mucosal pathogens theory.