Department of Periodontology, University of Florida, College of Dentistry, Gainesville, FL 32610, USA.
Cell Immunol. 2011;272(1):45-52. doi: 10.1016/j.cellimm.2011.09.008. Epub 2011 Sep 29.
Immune modulating factors are necessary for pathogen clearance, but also contribute to host tissues damage, as those seen in periodontal diseases. Many of these responses can be exacerbated by host conditions including type 2 diabetes [T2D], where toll-like receptor 4 [TLR4] and the receptor for advanced glycated end products [RAGE] play a significant role. Here we investigate causality associated with the increase in inflammatory markers observed in periodontally diseased patients with T2D using multi-variant correlation analysis. Inflammation associated with periodontal diseases, characterized by elevated pro-inflammatory cytokines, innate immune receptor expression, and cellular infiltrate was exacerbated in patients with T2D. In addition, a feed forward loop regulated by poor glycemic control was associated with a loss of mucosal barrier integrity and accumulation of innate immune receptor ligands resulting in an exacerbation of ongoing inflammation, where RAGE and TLR4 cooperated to induce responses in oral epithelial cells, which were exacerbated by hyperglycemia.
免疫调节因子对于清除病原体是必要的,但也会导致宿主组织损伤,如牙周病中所见。许多这些反应可能会被宿主状况加剧,包括 2 型糖尿病 [T2D],其中 Toll 样受体 4 [TLR4] 和晚期糖基化终产物受体 [RAGE] 发挥重要作用。在这里,我们使用多变量相关分析研究了与患有 T2D 的牙周病患者中观察到的炎症标志物增加相关的因果关系。与牙周病相关的炎症,其特征是促炎细胞因子、先天免疫受体表达和细胞浸润增加,在 T2D 患者中加剧。此外,由血糖控制不佳调节的正反馈回路与粘膜屏障完整性的丧失和先天免疫受体配体的积累有关,导致正在进行的炎症加剧,其中 RAGE 和 TLR4 合作诱导口腔上皮细胞产生反应,高血糖使其加剧。