Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement.
Low-abundance biofilm species orchestrates inflammatory periodontal disease through the commensal microbiota and complement.
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DOI：
10.1016/j.chom.2011.10.006
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发表时间：
2011-11-17
影响因子：
30.3
通讯作者：
Curtis MA
中科院分区：
文献类型：
--
作者：
Hajishengallis G;Liang S;Payne MA;Hashim A;Jotwani R;Eskan MA;McIntosh ML;Alsam A;Kirkwood KL;Lambris JD;Darveau RP;Curtis MA
牙龈卟啉单胞菌是一种低丰度的口腔厌氧细菌，与牙周炎、一种多菌炎性疾病及相关的全身疾病有关。然而，牙龈假单胞菌促进炎症和疾病的机制仍然不清楚。在这里，我们显示牙龈假单胞菌，在非常低的定植水平，触发了口腔共生微生物群的数量和组成的变化，导致炎症牙周骨丢失。无菌小鼠或C3a和C5a受体缺陷小鼠在接种牙龈假单胞菌后不会发生骨丢失，因此共生微生物群和补体途径都是牙龈假单胞菌诱导骨丢失所必需的。这些发现表明，单一的低丰度物种可以破坏宿主-微生物的动态平衡，从而导致炎症性疾病。对具有全社区影响的低丰度相似病原体的识别和靶向对于治疗多菌病原学的炎症性疾病可能是重要的。
Porphyromonas gingivalis is a low-abundance oral anaerobic bacterium implicated in periodontitis, a polymicrobial inflammatory disease, and the associated systemic conditions. However, the mechanism by which P. gingivalis contributes to inflammation and disease has remained elusive. Here we show that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss. The commensal microbiota and the complement pathway were both required for P. gingivalis-induced bone loss as germ-free mice or conventionally raised C3a and C5a receptor deficient mice did not develop bone loss after inoculation with P. gingivalis. These findings demonstrate that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease. The identification and targeting of similar low-abundance pathogens with community-wide impact may be important for treating inflammatory diseases of polymicrobial etiology.
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