Arimatsu Kei, Yamada Hitomi, Miyazawa Haruna, Minagawa Takayoshi, Nakajima Mayuka, Ryder Mark I, Gotoh Kazuyoshi, Motooka Daisuke, Nakamura Shota, Iida Tetsuya, Yamazaki Kazuhisa
1] Laboratory of Periodontology and Immunology, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan [2] Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Division of Periodontology, Department of Orofacial Sciences, School of Dentistry, University of California, San Francisco, USA.
Sci Rep. 2014 May 6;4:4828. doi: 10.1038/srep04828.
Periodontitis has been implicated as a risk factor for metabolic disorders such as type 2 diabetes, atherosclerotic vascular diseases, and non-alcoholic fatty liver disease. Although bacteremias from dental plaque and/or elevated circulating inflammatory cytokines emanating from the inflamed gingiva are suspected mechanisms linking periodontitis and these diseases, direct evidence is lacking. We hypothesize that disturbances of the gut microbiota by swallowed bacteria induce a metabolic endotoxemia leading metabolic disorders. To investigate this hypothesis, changes in the gut microbiota, insulin and glucose intolerance, and levels of tissue inflammation were analysed in mice after oral administration of Porphyromonas gingivalis, a representative periodontopathogens. Pyrosequencing revealed that the population belonging to Bacteroidales was significantly elevated in P. gingivalis-administered mice which coincided with increases in insulin resistance and systemic inflammation. In P. gingivalis-administered mice blood endotoxin levels tended to be higher, whereas gene expression of tight junction proteins in the ileum was significantly decreased. These results provide a new paradigm for the interrelationship between periodontitis and systemic diseases.
牙周炎已被认为是2型糖尿病、动脉粥样硬化性血管疾病和非酒精性脂肪性肝病等代谢紊乱的危险因素。虽然来自牙菌斑的菌血症和/或发炎牙龈产生的循环炎症细胞因子水平升高被怀疑是连接牙周炎和这些疾病的机制,但缺乏直接证据。我们假设,吞咽细菌引起的肠道微生物群紊乱会导致代谢性内毒素血症,进而引发代谢紊乱。为了验证这一假设,我们在给小鼠口服牙龈卟啉单胞菌(一种典型的牙周病原体)后,分析了小鼠肠道微生物群的变化、胰岛素和葡萄糖不耐受情况以及组织炎症水平。焦磷酸测序显示,在给予牙龈卟啉单胞菌的小鼠中,属于拟杆菌目的菌群数量显著增加,这与胰岛素抵抗和全身炎症的增加相一致。在给予牙龈卟啉单胞菌的小鼠中,血液内毒素水平往往较高,而回肠中紧密连接蛋白的基因表达显著降低。这些结果为牙周炎与全身性疾病之间的相互关系提供了一个新的范例。