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结扎诱导牙周炎的口腔微生物组和牙龈转录组图谱。

Oral Microbiome and Gingival Transcriptome Profiles of Ligature-Induced Periodontitis.

机构信息

Department of Biomedical Sciences, School of Dental Medicine, University of Nevada Las Vegas, Las Vegas, NV, USA.

Center for Oral Health Research, College of Dentistry, University of Kentucky, Lexington, KY, USA.

出版信息

J Dent Res. 2020 Jun;99(6):746-757. doi: 10.1177/0022034520906138. Epub 2020 Feb 19.

DOI:10.1177/0022034520906138
PMID:32075482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7243415/
Abstract

This investigation evaluated the relationship of the oral microbiome and gingival transcriptome in health and periodontitis in nonhuman primates (). Subgingival plaque samples and gingival biopsies were collected from healthy sites and at sites undergoing ligature-induced periodontitis. Microbial samples were analyzed with 16S amplicon sequencing to identify bacterial profiles in young (3 to 7 y) and adult (12 to 23 y) animals. The gingival transcriptome was determined with a microarray analysis and focused on the expression level of 452 genes that are associated with the development of inflammation and innate and adaptive immune responses. Of the 396 total operational taxonomic units (OTUs) identified across the samples, 81.8% were detected in the young group and 99.5% in the adult group. Nevertheless, 58 of the OTUs composed 88% of the signal in adults, and 49 OTUs covered 91% of the OTU readouts in the young group. Correlation analyses between the microbiome members and specific gingival genes showed a high number of significant bacteria-gene correlations in the young healthy tissues, which decreased by 75% in diseased tissues. In contrast, these correlations increased by 2.5-fold in diseased versus healthy tissues of adult animals. Complexes of bacteria were delineated that related to specific sets of immune genes, differing in health and disease and in the young versus adult animals. The correlated gene profiles demonstrated selected pathway overrepresentation related to particular bacterial complexes. These results provide novel insights into microbiome changes with disease and the relationship of these changes to specific gene profiles and likely biologic activities occurring in healthy and diseased gingival tissues in this human-like periodontitis model.

摘要

本研究评估了口腔微生物组与非人类灵长类动物健康和牙周炎牙龈转录组的关系。()从健康部位和正在发生结扎诱导牙周炎的部位采集龈下菌斑样本和牙龈活检样本。用 16S 扩增子测序分析微生物样本,以鉴定年轻(3 至 7 岁)和成年(12 至 23 岁)动物的细菌谱。用微阵列分析确定牙龈转录组,重点关注与炎症和先天及适应性免疫反应发展相关的 452 个基因的表达水平。在样本中鉴定出的 396 个总操作分类单元(OTU)中,81.8%在年轻组中检测到,99.5%在成年组中检测到。然而,58 个 OTU 组成了成年组中 88%的信号,49 个 OTU 涵盖了年轻组中 91%的 OTU 读数。微生物组成员与特定牙龈基因之间的相关性分析表明,年轻健康组织中存在大量显著的细菌-基因相关性,而在病变组织中减少了 75%。相比之下,成年动物病变组织中的这些相关性增加了 2.5 倍。与特定免疫基因相关的细菌复合物被划定,这些复合物在健康和疾病以及年轻和成年动物中存在差异。相关的基因图谱显示,与特定细菌复合物相关的特定途径过表达。这些结果为人类样牙周炎模型中疾病相关的微生物组变化及其与特定基因图谱的关系以及健康和患病牙龈组织中可能发生的特定生物学活动提供了新的见解。

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本文引用的文献

1
Microbiome Profiles of Ligature-Induced Periodontitis in Nonhuman Primates across the Life Span.生命全周期中非人类灵长类动物结扎诱导牙周炎的微生物组特征。
Infect Immun. 2019 May 21;87(6). doi: 10.1128/IAI.00067-19. Print 2019 Jun.
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A dysbiotic microbiome triggers T17 cells to mediate oral mucosal immunopathology in mice and humans.肠道菌群失调会触发 T17 细胞,介导小鼠和人类口腔黏膜免疫病理学。
Sci Transl Med. 2018 Oct 17;10(463). doi: 10.1126/scitranslmed.aat0797.
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Clinical and microbiological parameters of naturally occurring periodontitis in the non-human primate .非人灵长类动物自然发生的牙周炎的临床和微生物学参数
J Oral Microbiol. 2017 Nov 25;9(1):1403843. doi: 10.1080/20002297.2017.1403843. eCollection 2017.
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Gene expression analysis of neuropeptides in oral mucosa during periodontal disease in non-human primates.口腔黏膜神经肽在非人类灵长类牙周病中的基因表达分析。
J Periodontol. 2018 Jul;89(7):858-866. doi: 10.1002/JPER.17-0521. Epub 2018 Jul 20.
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Periodontal profile classes predict periodontal disease progression and tooth loss.牙周状况分类可预测牙周病的进展和牙齿丧失。
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Br Dent J. 2016 Nov 18;221(10):657-666. doi: 10.1038/sj.bdj.2016.865.
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IL-17: overview and role in oral immunity and microbiome.IL-17:概述及其在口腔免疫和微生物组中的作用。
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The subgingival periodontal microbiota of the aging mouth.衰老口腔的龈下牙周微生物群
Periodontol 2000. 2016 Oct;72(1):30-53. doi: 10.1111/prd.12136.