The inflammophilic character of the periodontitis-associated microbiota.
The inflammophilic character of the periodontitis-associated microbiota.
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DOI：
10.1111/omi.12065
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发表时间：
2014-12
影响因子：
3.7
通讯作者：
Hajishengallis G
中科院分区：
文献类型：
--
作者：
Hajishengallis G
在牙周炎中，益生菌群落表现出协同相互作用，以增强宿主防御，营养获取和炎症环境中的持久性。这篇综述讨论了牙周炎相关群落是“亲炎”的证据（=喜欢或吸引炎症），因为它们已经进化到不仅能忍受炎症，而且能利用炎症。在这方面，炎症可以通过提供组织分解产物形式的营养来源（例如，降解的胶原肽和含血红素的化合物）来驱动这些致病群落的选择和富集。相反，那些不能从炎症环境改变的生态条件中受益的物种，或者对宿主炎症有害的物种，很可能会被淘汰。与炎症促进益生菌群落生长的概念一致，人类牙周炎相关生物膜的细菌生物量显示随着牙周炎症的增加而增加。相反，在牙周炎动物模型中，抗炎治疗显示除了防止骨质流失外，还能减少牙周细菌负荷。嗜炎细菌的选择性繁殖可以通过引发疾病进展的“恶性循环”，使炎症组织持续破坏，在这种恶性循环中，生态失调和炎症相互加强。因此，控制炎症似乎是牙周炎治疗的核心，因为它可能控制生态失调和疾病进展。
In periodontitis, dysbiotic microbial communities exhibit synergistic interactions for enhanced protection from host defenses, nutrient acquisition, and persistence in an inflammatory environment. This Review discusses evidence that periodontitis-associated communities are ‘inflammo-philic’ (= loving or attracted to inflammation) in that they have evolved to not only endure inflammation but also to take advantage of it. In this regard, inflammation can drive the selection and enrichment of these pathogenic communities by providing a source of nutrients in the form of tissue breakdown products (e.g., degraded collagen peptides and heme-containing compounds). In contrast, those species that cannot benefit from the altered ecological conditions of the inflammatory environment, or for which host inflammation is detrimental, are likely to be outcompeted. Consistent with the concept that inflammation fosters the growth of dysbiotic microbial communities, the bacterial biomass of human periodontitis-associated biofilms was shown to increase with increasing periodontal inflammation. Conversely, anti-inflammatory treatments in animal models of periodontitis were shown to diminish the periodontal bacterial load, in addition to protecting from bone loss. The selective flourishing of inflammophilic bacteria can perpetuate inflammatory tissue destruction by setting off a ‘vicious cycle’ for disease progression, in which dysbiosis and inflammation reinforce each other. Therefore, the control of inflammation appears to be central to the treatment of periodontitis, as it is likely to control both dysbiosis and disease progression.
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影响因子：
11
作者：
Duran-Pinedo, Ana E.;Chen, Tsute;Frias-Lopez, Jorge
通讯作者：
Frias-Lopez, Jorge
影响因子：
30.5
作者：
通讯作者：
--
Keystone-Pathogen假设。
DOI：
10.1038/nrmicro2873
发表时间：
2012-10
期刊：
Nature reviews. Microbiology
影响因子：
--
作者：
通讯作者：
--
DOI：
10.4049/jimmunol.1202339
发表时间：
2012-12-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Abe T;Hosur KB;Hajishengallis E;Reis ES;Ricklin D;Lambris JD;Hajishengallis G
通讯作者：
Hajishengallis G
影响因子：
6.7
作者：
Chaves, ES;Jeffcoat, MK;Snyder, B
通讯作者：
Snyder, B