Department of Pharmacology and Nutritional Sciences and Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, USA.
Department of Oral Health Practice, Division of Periodontology, College of Dentistry, University of Kentucky, Lexington, KY, USA.
Adv Exp Med Biol. 2019;1197:45-54. doi: 10.1007/978-3-030-28524-1_4.
New strategies are critically needed to counter uncontrolled periodontal infection and inflammation in obesity-associated type 2 diabetes (T2D). However, mechanisms that explain the relationship between periodontitis (PD) and T2D remain poorly understood. Several lines of evidence indicate that destructive immune responses potentiate periodontitis (PD) in T2D. B cells are abundant in periodontal lesions, and our data show that B cells are required for PD in obese/insulin resistant but not lean/normoglycemic mice. In mice and in people, T2D-primed B cells supported Th17 cytokine profiles, but B cells had a modest effect on T-cell function in samples from normoglycemic individuals. Given the recently appreciated importance of Th17 cells in PD outside a T2D milieu, our data raise the possibility that B cells indirectly promote T2D-potentiated PD through support of Th17 cells, which in turn directly promote PD.Data herein thereby suggest unexpected mechanisms that explain the clinical observation that T2D potentiates PD.
需要新的策略来对抗肥胖相关 2 型糖尿病(T2D)中不受控制的牙周感染和炎症。然而,解释牙周炎(PD)与 T2D 之间关系的机制仍知之甚少。有几条证据表明,破坏性免疫反应增强了 T2D 中的牙周炎(PD)。B 细胞在牙周病变中大量存在,我们的数据表明,B 细胞是肥胖/胰岛素抵抗小鼠而非瘦/正常血糖小鼠 PD 所必需的。在小鼠和人类中,T2D 预致敏的 B 细胞支持 Th17 细胞因子谱,但 B 细胞对正常血糖个体样本中的 T 细胞功能的影响较小。鉴于最近在 T2D 环境之外的 PD 中 Th17 细胞的重要性,我们的数据提出了一种可能性,即 B 细胞通过支持 Th17 细胞间接促进 T2D 增强的 PD,而 Th17 细胞反过来又直接促进 PD。因此,这些数据提出了一些意想不到的机制来解释临床观察到的 T2D 增强 PD 的现象。