Human variation in gingival inflammation.
Human variation in gingival inflammation.
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DOI：
10.1073/pnas.2012578118
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发表时间：
2021-07-06
影响因子：
11.1
通讯作者：
Darveau RP
中科院分区：
文献类型：
--
作者：
Bamashmous S;Kotsakis GA;Kerns KA;Leroux BG;Zenobia C;Chen D;Trivedi HM;McLean JS;Darveau RP
实验性牙龈炎研究中，某些牙齿不进行牙齿卫生，从而导致细菌自然积累，这为研究人类从健康到炎症性疾病的可逆转变提供了独特的机会。对人类实验性牙龈炎期间微生物和宿主变化的纵向分析揭示了炎症期间人类宿主反应和微生物演替顺序的先前未知的变化。我们的发现的意义可以概括为两个要点。首先，该研究全面描述了三种不同的临床反应（指定为高、低和慢），区分了定义每个组的独特宿主和微生物特征。其次，我们揭示了以前未被认识的宿主保护机制，以防止可逆性牙龈炎症期间的炎性骨吸收。口腔共生细菌积极参与牙龈组织，以维持健康的中性粒细胞监测以及正常的组织和骨转换过程。这种宿主与细菌稳态关系的破坏发生在实验性牙龈炎研究中，已明确证实细菌负荷的增加会加剧牙龈炎症。在这里，我们证明实验性牙龈炎导致三种独特的临床炎症表型（高、低和慢），并揭示白细胞介素-1β（一种报道的与牙龈炎相关的主要炎症介质）与慢反应组的临床牙龈炎症无关。此外，链球菌属的水平显着升高。对于这个群体来说也是独一无二的。低临床反应组的特点是宿主介质浓度低，尽管细菌积累和组成特征与高临床反应组相似。所有反应组中的中性粒细胞和骨活化调节剂均下调，揭示了牙龈炎症期间新的组织和骨保护反应。实验性牙龈炎期间趋化因子和微生物组成反应的这些变化揭示了人类宿主对牙龈稳态破坏的反应中以前未表征的变化。了解人类牙龈炎症的差异可能有助于识别牙周炎易感人群。总体而言，这项研究强调了由于宿主免疫特征（低反应者）和微生物群落成熟（慢反应者）的变化而引起的人群宿主反应的变异性，这可能会影响破坏性炎症方面的临床结果。
Experimental gingivitis studies where dental hygiene is withheld from select teeth, allowing natural bacterial accumulation, provide a unique opportunity to study the reversible transition from health to inflammatory disease in humans. Longitudinal analysis of both the microbial and host changes during human experimental gingivitis revealed a previously unknown variation in the human host response and microbial succession sequence during inflammation. The significance of our findings can be summarized in two major points. First, the study comprehensively characterizes three different clinical responses—designated high, low, and slow—discerning unique host and microbial features that define each group. Second, we have unveiled previously unrecognized host protective mechanisms to prevent inflammatory bone resorption during reversible gingival inflammation. Oral commensal bacteria actively participate with gingival tissue to maintain healthy neutrophil surveillance and normal tissue and bone turnover processes. Disruption of this homeostatic host–bacteria relationship occurs during experimental gingivitis studies where it has been clearly established that increases in the bacterial burden increase gingival inflammation. Here, we show that experimental gingivitis resulted in three unique clinical inflammatory phenotypes (high, low, and slow) and reveal that interleukin-1β, a reported major gingivitis-associated inflammatory mediator, was not associated with clinical gingival inflammation in the slow response group. In addition, significantly higher levels of Streptococcus spp. were also unique to this group. The low clinical response group was characterized by low concentrations of host mediators, despite similar bacterial accumulation and compositional characteristics as the high clinical response group. Neutrophil and bone activation modulators were down-regulated in all response groups, revealing novel tissue and bone protective responses during gingival inflammation. These alterations in chemokine and microbial composition responses during experimental gingivitis reveal a previously uncharacterized variation in the human host response to a disruption in gingival homeostasis. Understanding this human variation in gingival inflammation may facilitate the identification of periodontitis-susceptible individuals. Overall, this study underscores the variability in host responses in the human population arising from variations in host immune profiles (low responders) and microbial community maturation (slow responders) that may impact clinical outcomes in terms of destructive inflammation.
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影响因子：
3.7
作者：
Hajishengallis G
通讯作者：
Hajishengallis G
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：
--
影响因子：
48
作者：
Callahan BJ;McMurdie PJ;Rosen MJ;Han AW;Johnson AJ;Holmes SP
通讯作者：
Holmes SP
影响因子：
3.1
作者：
Darveau, Richard P.
通讯作者：
Darveau, Richard P.
影响因子：
4.3
作者：
Chang, Ana M.;Liu, Quanhui;Darveau, Richard P.
通讯作者：
Darveau, Richard P.