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Phylogenetic and functional gene structure shifts of the oral microbiomes in periodontitis patients

Identifieur interne : 000009 ( Pmc/Corpus ); précédent : 000008; suivant : 000010

Phylogenetic and functional gene structure shifts of the oral microbiomes in periodontitis patients

Auteurs : Yan Li ; Jinzhi He ; Zhili He ; Yuan Zhou ; Mengting Yuan ; Xin Xu ; Feifei Sun ; Chengcheng Liu ; Jiyao Li ; Wenbo Xie ; Ye Deng ; Yujia Qin ; Joy D. Vannostrand ; Liying Xiao ; Liyou Wu ; Jizhong Zhou ; Wenyuan Shi ; Xuedong Zhou

Source :

RBID : PMC:4139721

Abstract

Determining the composition and function of subgingival dental plaque is crucial to understanding human periodontal health and disease, but it is challenging because of the complexity of the interactions between human microbiomes and human body. Here, we examined the phylogenetic and functional gene differences between periodontal and healthy individuals using MiSeq sequencing of 16S rRNA gene amplicons and a specific functional gene array (a combination of GeoChip 4.0 for biogeochemical processes and HuMiChip 1.0 for human microbiomes). Our analyses indicated that the phylogenetic and functional gene structure of the oral microbiomes were distinctly different between periodontal and healthy groups. Also, 16S rRNA gene sequencing analysis indicated that 39 genera were significantly different between healthy and periodontitis groups, and Fusobacterium, Porphyromonas, Treponema, Filifactor, Eubacterium, Tannerella, Hallella, Parvimonas, Peptostreptococcus and Catonella showed higher relative abundances in the periodontitis group. In addition, functional gene array data showed that a lower gene number but higher signal intensity of major genes existed in periodontitis, and a variety of genes involved in virulence factors, amino acid metabolism and glycosaminoglycan and pyrimidine degradation were enriched in periodontitis, suggesting their potential importance in periodontal pathogenesis. However, the genes involved in amino acid synthesis and pyrimidine synthesis exhibited a significantly lower relative abundance compared with healthy group. Overall, this study provides new insights into our understanding of phylogenetic and functional gene structure of subgingival microbial communities of periodontal patients and their importance in pathogenesis of periodontitis.


Url:
DOI: 10.1038/ismej.2014.28
PubMed: 24671083
PubMed Central: 4139721

Links to Exploration step

PMC:4139721

Le document en format XML

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<p>Determining the composition and function of subgingival dental plaque is crucial to understanding human periodontal health and disease, but it is challenging because of the complexity of the interactions between human microbiomes and human body. Here, we examined the phylogenetic and functional gene differences between periodontal and healthy individuals using MiSeq sequencing of 16S rRNA gene amplicons and a specific functional gene array (a combination of GeoChip 4.0 for biogeochemical processes and HuMiChip 1.0 for human microbiomes). Our analyses indicated that the phylogenetic and functional gene structure of the oral microbiomes were distinctly different between periodontal and healthy groups. Also, 16S rRNA gene sequencing analysis indicated that 39 genera were significantly different between healthy and periodontitis groups, and
<italic>Fusobacterium</italic>
,
<italic>Porphyromonas</italic>
,
<italic>Treponema</italic>
,
<italic>Filifactor</italic>
,
<italic>Eubacterium</italic>
,
<italic>Tannerella</italic>
,
<italic>Hallella</italic>
,
<italic>Parvimonas</italic>
,
<italic>Peptostreptococcus</italic>
and
<italic>Catonella</italic>
showed higher relative abundances in the periodontitis group. In addition, functional gene array data showed that a lower gene number but higher signal intensity of major genes existed in periodontitis, and a variety of genes involved in virulence factors, amino acid metabolism and glycosaminoglycan and pyrimidine degradation were enriched in periodontitis, suggesting their potential importance in periodontal pathogenesis. However, the genes involved in amino acid synthesis and pyrimidine synthesis exhibited a significantly lower relative abundance compared with healthy group. Overall, this study provides new insights into our understanding of phylogenetic and functional gene structure of subgingival microbial communities of periodontal patients and their importance in pathogenesis of periodontitis.</p>
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<surname>Li</surname>
<given-names>Yan</given-names>
</name>
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<sup>4</sup>
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<given-names>Jinzhi</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
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<sup>4</sup>
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<name>
<surname>He</surname>
<given-names>Zhili</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhou</surname>
<given-names>Yuan</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
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<name>
<surname>Yuan</surname>
<given-names>Mengting</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
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<name>
<surname>Xu</surname>
<given-names>Xin</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
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<contrib contrib-type="author">
<name>
<surname>Sun</surname>
<given-names>Feifei</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Liu</surname>
<given-names>Chengcheng</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Li</surname>
<given-names>Jiyao</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
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<contrib contrib-type="author">
<name>
<surname>Xie</surname>
<given-names>Wenbo</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Deng</surname>
<given-names>Ye</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Qin</surname>
<given-names>Yujia</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>VanNostrand</surname>
<given-names>Joy D</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Xiao</surname>
<given-names>Liying</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Wu</surname>
<given-names>Liyou</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhou</surname>
<given-names>Jizhong</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
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<contrib contrib-type="author">
<name>
<surname>Shi</surname>
<given-names>Wenyuan</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff3">3</xref>
<xref ref-type="corresp" rid="caf1">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Zhou</surname>
<given-names>Xuedong</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="caf2">*</xref>
</contrib>
<aff id="aff1">
<label>1</label>
<institution>State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University</institution>
, Chengdu,
<country>China</country>
</aff>
<aff id="aff2">
<label>2</label>
<institution>Institute for Environmental Genomics, Department of Microbiology and Plant Biology, University of Oklahoma</institution>
, Norman, OK,
<country>USA</country>
</aff>
<aff id="aff3">
<label>3</label>
<institution>UCLA School of Dentistry</institution>
, Los Angeles, CA,
<country>USA</country>
</aff>
</contrib-group>
<author-notes>
<corresp id="caf1">
<label>*</label>
<institution>UCLA School of Dentistry</institution>
, 10833 Le Conte Avenue, CHS 20-118, Los Angeles, CA 90095-1668,
<country>USA</country>
. E-mail:
<email>wenyuan@ucla.edu</email>
</corresp>
<corresp id="caf2">
<label>*</label>
<institution>State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University</institution>
, Chengdu 610041,
<country>China</country>
. E-mail:
<email>zhouxd@scu.edu.cn</email>
</corresp>
<fn fn-type="present-address" id="note1">
<label>4</label>
<p>These two authors contributed equally to this work.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub">
<month>09</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub">
<day>27</day>
<month>03</month>
<year>2014</year>
</pub-date>
<volume>8</volume>
<issue>9</issue>
<fpage>1879</fpage>
<lpage>1891</lpage>
<history>
<date date-type="received">
<day>02</day>
<month>07</month>
<year>2013</year>
</date>
<date date-type="rev-recd">
<day>09</day>
<month>12</month>
<year>2013</year>
</date>
<date date-type="accepted">
<day>25</day>
<month>01</month>
<year>2014</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright © 2014 International Society for Microbial Ecology</copyright-statement>
<copyright-year>2014</copyright-year>
<copyright-holder>International Society for Microbial Ecology</copyright-holder>
</permissions>
<abstract>
<p>Determining the composition and function of subgingival dental plaque is crucial to understanding human periodontal health and disease, but it is challenging because of the complexity of the interactions between human microbiomes and human body. Here, we examined the phylogenetic and functional gene differences between periodontal and healthy individuals using MiSeq sequencing of 16S rRNA gene amplicons and a specific functional gene array (a combination of GeoChip 4.0 for biogeochemical processes and HuMiChip 1.0 for human microbiomes). Our analyses indicated that the phylogenetic and functional gene structure of the oral microbiomes were distinctly different between periodontal and healthy groups. Also, 16S rRNA gene sequencing analysis indicated that 39 genera were significantly different between healthy and periodontitis groups, and
<italic>Fusobacterium</italic>
,
<italic>Porphyromonas</italic>
,
<italic>Treponema</italic>
,
<italic>Filifactor</italic>
,
<italic>Eubacterium</italic>
,
<italic>Tannerella</italic>
,
<italic>Hallella</italic>
,
<italic>Parvimonas</italic>
,
<italic>Peptostreptococcus</italic>
and
<italic>Catonella</italic>
showed higher relative abundances in the periodontitis group. In addition, functional gene array data showed that a lower gene number but higher signal intensity of major genes existed in periodontitis, and a variety of genes involved in virulence factors, amino acid metabolism and glycosaminoglycan and pyrimidine degradation were enriched in periodontitis, suggesting their potential importance in periodontal pathogenesis. However, the genes involved in amino acid synthesis and pyrimidine synthesis exhibited a significantly lower relative abundance compared with healthy group. Overall, this study provides new insights into our understanding of phylogenetic and functional gene structure of subgingival microbial communities of periodontal patients and their importance in pathogenesis of periodontitis.</p>
</abstract>
<kwd-group>
<kwd>functional gene array</kwd>
<kwd>Illumina sequencing</kwd>
<kwd>periodontitis</kwd>
<kwd>subgingival dental plaque</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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