Anna Karenina and the subgingival microbiome associated with periodontitis.
Anna Karenina and the subgingival microbiome associated with periodontitis.
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Anna Karenina和与牙周炎相关的副因微生物组。
DOI：
10.1186/s40168-021-01056-3
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发表时间：
2021-04-30
期刊：
影响因子：
15.5
通讯作者：
Kumar PS
中科院分区：
文献类型：
--
作者：
Altabtbaei K;Maney P;Ganesan SM;Dabdoub SM;Nagaraja HN;Kumar PS
尽管局部侵袭性牙周炎 (LAP)、广泛性侵袭性牙周炎 (GAP) 和慢性牙周炎 (CP) 是微生物驱动的疾病，但我们无法将疾病特异性关联与所有三种形式的牙周炎共有的关联区分开来，这阻碍了生物标志物的发现。因此，我们的目的是绘制与这些临床表型相关的微生物组的基因组内容以及由其编码的生物途径。我们还估计了这些生物群落受安娜卡列尼娜原则（AKP）支配的程度，该原则指出，个体之间的优生群落是相似的，而与疾病相关的群落是高度个体化的。我们从 25 名牙周健康个体和 59 名 3 期牙周炎受试者的患病部位收集了龈下菌斑，并使用鸟枪法宏基因组学来表征细菌基因的聚集。 Beta 分散度指标表明 AKP 在 CP 中最为明显，其次是 GAP 和 LAP。我们发现了跨越三种表型的广泛的生态失调特征，过度代表性的途径促进了缺氧、富含蛋白质和血红素的促氧化环境中的生命，并增强了附着和生物膜形成的能力。 LAP 微生物组中的表型特异性指标比 GAP 或 CP 更明显。能够清除乙酸盐的生活方式、利用替代营养来源、氧化和亚硝化应激反应以及铁载体产生的基因是 LAP 所独有的。从 LAP 到 GAP 再到 CP，毒力相关功能和应激反应的减弱是明显的。我们还发现，疾病的临床表型比新建立的分级系统更清晰地解决了微生物组的差异。重要的是，我们观察到 LAP 宏基因组的三分之一是该表型所独有的，而 GAP 与 LAP 和 CP 具有显着的功能和分类特征，表明侵袭性疾病或早发慢性疾病的减弱。在小样本量和横断面研究设计的限制下，与 LAP 和 CP 相关的微生物组的独特特征强烈地说服我们，这些是离散的疾病实体，同时质疑 GAP 是否是一种单独的疾病，还是由横断面研究设计引起的人为因素。有必要对表型特异性微生物基因进行进一步研究，以阐明它们在疾病病因学中的作用。视频摘要 在线版本包含可在 10.1186/s40168-021-01056-3 获取的补充材料。
Although localized aggressive periodontitis (LAP), generalized aggressive periodontitis (GAP), and chronic periodontitis (CP) are microbially driven diseases, our inability to separate disease-specific associations from those common to all three forms of periodontitis has hampered biomarker discovery. Therefore, we aimed to map the genomic content of, and the biological pathways encoded by, the microbiomes associated with these clinical phenotypes. We also estimated the extent to which these biomes are governed by the Anna Karenina principle (AKP), which states that eubiotic communities are similar between individuals while disease-associated communities are highly individualized. We collected subgingival plaque from 25 periodontally healthy individuals and diseased sites of 59 subjects with stage 3 periodontitis and used shotgun metagenomics to characterize the aggregate of bacterial genes. Beta-dispersion metrics demonstrated that AKP was most evident in CP, followed by GAP and LAP. We discovered broad dysbiotic signatures spanning the three phenotypes, with over-representation of pathways that facilitate life in an oxygen-poor, protein- and heme-rich, pro-oxidant environment and enhance capacity for attachment and biofilm formation. Phenotype-specific indicators were more readily evident in LAP microbiome than GAP or CP. Genes that enable acetate-scavenging lifestyle, utilization of alternative nutritional sources, oxidative and nitrosative stress responses, and siderophore production were unique to LAP. An attenuation of virulence-related functionalities and stress response from LAP to GAP to CP was apparent. We also discovered that clinical phenotypes of disease resolved variance in the microbiome with greater clarity than the newly established grading system. Importantly, we observed that one third of the metagenome of LAP is unique to this phenotype while GAP shares significant functional and taxonomic features with both LAP and CP, suggesting either attenuation of an aggressive disease or an early-onset chronic disease. Within the limitations of a small sample size and a cross-sectional study design, the distinctive features of the microbiomes associated with LAP and CP strongly persuade us that these are discrete disease entities, while calling into question whether GAP is a separate disease, or an artifact induced by cross-sectional study designs. Further studies on phenotype-specific microbial genes are warranted to explicate their role in disease etiology. Video Abstract The online version contains supplementary material available at 10.1186/s40168-021-01056-3.
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