Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Institute of Stomatological Research, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, China.
Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Front Cell Infect Microbiol. 2021 Dec 1;11:755925. doi: 10.3389/fcimb.2021.755925. eCollection 2021.
Periodontal pathogen and gut microbiota are closely associated with the pathogenesis of Alzheimer's disease (AD). (Pg), the keystone periodontal pathogen, can induce cognitive impairment. The gut has a connection and communication with the brain, which is an important aspect of the gut-brain axis (GBA). In the present study, we investigate whether Pg induces cognitive impairment through disturbing the GBA.
In this study, Pg was orally administered to mice, three times a week for 1 month. The effects of Pg administration on the gut and brain were evaluated through behaviors, gut microbiota, immune cells, glymphatic pathway clearance, and neuroinflammation.
Pg induced cognitive impairment and dysbiosis of gut microbiota. The α-diversity parameters did not show significant change after Pg administration. The β-diversity demonstrated that the gut microbiota compositions were different between the Pg-administered and control groups. At the species level, the Pg group displayed a lower abundance of and than the control group, but a higher abundance of . The proportions of lymphocytes in the periphery and myeloid cells infiltrating the brain were increased in Pg-treated animals. In addition, the solute clearance efficiency of the glymphatic system decreased. Neurons in the hippocampus and cortex regions were reduced in mice treated with Pg. Microglia, astrocytes, and apoptotic cells were increased. Furthermore, amyloid plaque appeared in the hippocampus and cortex regions in Pg-treated mice.
These findings indicate that Pg may play an important role in gut dysbiosis, neuroinflammation, and glymphatic system impairment, which may in turn lead to cognitive impairment.
牙周病原体和肠道微生物群与阿尔茨海默病（AD）的发病机制密切相关。牙龈卟啉单胞菌（Pg），作为关键的牙周病原体，可引起认知障碍。肠道与大脑相连并进行交流，这是肠脑轴（GBA）的一个重要方面。在本研究中，我们研究了 Pg 是否通过干扰 GBA 引起认知障碍。
在这项研究中，Pg 经口给予小鼠，每周 3 次，持续 1 个月。通过行为、肠道微生物群、免疫细胞、糖质淋系统清除和神经炎症来评估 Pg 给药对肠道和大脑的影响。
Pg 诱导认知障碍和肠道微生物群失调。Pg 给药后α多样性参数没有显著变化。β多样性表明 Pg 给药组和对照组的肠道微生物群组成不同。在物种水平上，Pg 组的 和 的丰度低于对照组，而 的丰度高于对照组。外周血淋巴细胞和浸润大脑的髓样细胞的比例在 Pg 处理的动物中增加。此外，糖质淋系统的溶质清除效率降低。在 Pg 处理的小鼠中，海马和皮质区域的神经元减少。小胶质细胞、星形胶质细胞和凋亡细胞增加。此外，在 Pg 处理的小鼠的海马和皮质区域出现了淀粉样斑块。
这些发现表明 Pg 可能在肠道菌群失调、神经炎症和糖质淋系统损伤中发挥重要作用，进而导致认知障碍。
