発電機能を持つ歯周病細菌におけると鉄イオン排出機構に関する研究

牙龈卟啉单胞菌（Porphyromonasgingivalis，PG）是牙菌斑生物膜的典型成员。PG是与慢性口腔疾病和全身性炎症性疾病如心血管、关节炎和神经退行性疾病相关的关键病原体。本研究旨在确定EET偶联PG中铁输出导致炎症和腐蚀的关键机制。PG能吸收可溶性Fe ~（2+），并以氧化态Fe ~（3+）的形式储存在细胞内，以备缺铁时利用。然而，虽然必须避免由于过量的铁，PG铁稳态和输出机制的毒性还没有得到很好的理解。本研究比较了PG在不同氨基底物作用下的胞外电子转运能力。与其他底物相比，牙龈卟啉单胞菌的库仑效率（CE）为2.8%，显著增加了组氨酸代谢的电流，这比之前报道的牙龈卟啉单胞菌对葡萄糖氧化的CE（0.003%）高出约1000倍。在本研究中，对牙龈卟啉单胞菌铁还原的重要鉴定进行了测试和鉴定，表明EET与牙龈卟啉单胞菌铁还原偶联的可能机制。铁对病原菌生长的影响也表现在电子传递能力上。我们的研究结果表明，氨基酸，特别是组氨酸，其电流产生速率是葡萄糖的8倍，可以作为溶砷病原体牙龈卟啉单胞菌的碳源。

Porphyromonas gingivalis (PG) is a typical member of the dental plaque biofilm found on the tooth surface. PG is a keystone pathogen associated with chronic oral diseases and systemic inflammatory disorders such as cardiovascular, arthritic, and neurodegenerative diseases. This research aims to identify the critical mechanisms of EET coupled iron export in PG leading to inflammation and corrosion. PG can take up soluble Fe2+ and store it in oxidized Fe3+ form intracellularly to utilize in times of iron limitation. However, whilst essential to avoid toxicity due to excess iron, PG iron homeostasis and the export mechanism is not well understood. This study investigated and compared the extracellular elecctron transport (EET) capabilities of PG using various amino substrates. With a coulombic efficiency (CE) of 2.8%, P. gingivalis considerably increased current with histidine metabolism compared to other substrates, which is around 1000 times higher than the CE that P. gingivalis was previously reported to have for glucose oxidation (0.003%). During this research, important identification of Iron reduction by P. gingivalis was tested and identified the same, indicating the possible mechanism of EET coupled with Iron reduction by P. gingivalis. And iron has showed the impact on the growth of pathogen reflected in the electron transfer capability as well. Our findings demonstrate that amino acids, particularly histidine, which has an eight times greater current production rate than glucose, can serve as carbon sources for the asaccharolytic pathogen P. gingivalis.