Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status
Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to a...
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creator | Corrêa, Jôice Dias Calderaro, Débora Cerqueira Ferreira, Gilda Aparecida Mendonça, Santuza Maria Souza Fernandes, Gabriel R Xiao, E Teixeira, Antônio Lúcio Leys, Eugene J Graves, Dana T Silva, Tarcília Aparecida |
description | Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to affect the subgingival microbiota and clinical periodontal status. However, this relationship has not been examined in subjects with systemic lupus erythematosus (SLE). The objective of our study was to investigate the influence of SLE on the subgingival microbiota and its connection with periodontal disease and SLE activity.
We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing.
SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis.
SLE is associated with differences in the composition of the microbiota, independently of periodontal status. |
doi_str_mv | 10.1186/s40168-017-0252-z |
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We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing.
SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis.
SLE is associated with differences in the composition of the microbiota, independently of periodontal status.</description><identifier>ISSN: 2049-2618</identifier><identifier>EISSN: 2049-2618</identifier><identifier>DOI: 10.1186/s40168-017-0252-z</identifier><identifier>PMID: 28320468</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Adult ; Autoimmune diseases ; Bacteria - classification ; Bacteria - genetics ; Bacteria - isolation & purification ; Bacteroides - genetics ; Dental plaque ; Dental Plaque - microbiology ; Dysbiosis ; Female ; Gingiva - microbiology ; Gum disease ; High-Throughput Nucleotide Sequencing ; Humans ; Hypothesis testing ; Immunology ; Inflammatory diseases ; Interleukin-17 - immunology ; Interleukin-17 - metabolism ; Interleukin-33 - immunology ; Interleukin-33 - metabolism ; Interleukin-6 - immunology ; Interleukin-6 - metabolism ; Lupus ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - microbiology ; Male ; Microbiota ; Microbiota - genetics ; Middle Aged ; Periodontics ; Periodontitis - immunology ; Periodontitis - microbiology ; Rheumatic diseases ; Rheumatoid arthritis ; Rheumatology ; RNA, Ribosomal, 16S - genetics ; Systemic lupus erythematosus ; Teeth ; Young Adult</subject><ispartof>Microbiome, 2017-03, Vol.5 (1), p.34-34, Article 34</ispartof><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-b0ef8fd7168319e82a3dbad6216c5a8f78c305d8876016968d603acb9e8f875a3</citedby><cites>FETCH-LOGICAL-c427t-b0ef8fd7168319e82a3dbad6216c5a8f78c305d8876016968d603acb9e8f875a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5359961/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5359961/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28320468$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Corrêa, Jôice Dias</creatorcontrib><creatorcontrib>Calderaro, Débora Cerqueira</creatorcontrib><creatorcontrib>Ferreira, Gilda Aparecida</creatorcontrib><creatorcontrib>Mendonça, Santuza Maria Souza</creatorcontrib><creatorcontrib>Fernandes, Gabriel R</creatorcontrib><creatorcontrib>Xiao, E</creatorcontrib><creatorcontrib>Teixeira, Antônio Lúcio</creatorcontrib><creatorcontrib>Leys, Eugene J</creatorcontrib><creatorcontrib>Graves, Dana T</creatorcontrib><creatorcontrib>Silva, Tarcília Aparecida</creatorcontrib><title>Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status</title><title>Microbiome</title><addtitle>Microbiome</addtitle><description>Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to affect the subgingival microbiota and clinical periodontal status. However, this relationship has not been examined in subjects with systemic lupus erythematosus (SLE). The objective of our study was to investigate the influence of SLE on the subgingival microbiota and its connection with periodontal disease and SLE activity.
We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing.
SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis.
SLE is associated with differences in the composition of the microbiota, independently of periodontal status.</description><subject>Adult</subject><subject>Autoimmune diseases</subject><subject>Bacteria - classification</subject><subject>Bacteria - genetics</subject><subject>Bacteria - isolation & purification</subject><subject>Bacteroides - genetics</subject><subject>Dental plaque</subject><subject>Dental Plaque - microbiology</subject><subject>Dysbiosis</subject><subject>Female</subject><subject>Gingiva - microbiology</subject><subject>Gum disease</subject><subject>High-Throughput Nucleotide Sequencing</subject><subject>Humans</subject><subject>Hypothesis testing</subject><subject>Immunology</subject><subject>Inflammatory diseases</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-33 - immunology</subject><subject>Interleukin-33 - metabolism</subject><subject>Interleukin-6 - immunology</subject><subject>Interleukin-6 - metabolism</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - microbiology</subject><subject>Male</subject><subject>Microbiota</subject><subject>Microbiota - genetics</subject><subject>Middle Aged</subject><subject>Periodontics</subject><subject>Periodontitis - immunology</subject><subject>Periodontitis - microbiology</subject><subject>Rheumatic diseases</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>RNA, Ribosomal, 16S - genetics</subject><subject>Systemic lupus erythematosus</subject><subject>Teeth</subject><subject>Young Adult</subject><issn>2049-2618</issn><issn>2049-2618</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkU9P3DAQxa2KqiDKB-gFWeqFS1r_SWynh0oIQVsJiQP0bDmJs2uUxFuPDVo-PYMWENQXjzS_eZo3j5AvnH3j3KjvUDOuTMW4rphoRPXwgRwIVreVUNzsvan3yRHALcPX8lrX5hPZF0ZiW5kD4q9LtwrLKty5ic6hT7ELMTs6bAELCEDDQmEL2WOTTmVTgPq0zWs_uxyhwA_qAGIfXA5xofchr-nGpxCHuGSUhOxygc_k4-gm8EfP_yH5e3F-c_a7urz69efs9LLqa6Fz1TE_mnHQ6Evy1hvh5NC5QQmu-saZUZtesmYwRiv03iozKCZd3yE6Gt04eUh-7nQ3pZv90PslJzfZTQqzS1sbXbDvO0tY21W8s41s2lZxFDh5FkjxX_GQ7Ryg99PkFh8LWG50q5TGBRD9-h96G0ta0B5SppZG4I2R4jsKLwuQ_Pi6DGf2KUe7y9FijvYpR_uAM8dvXbxOvKQmHwHbC5w_</recordid><startdate>20170320</startdate><enddate>20170320</enddate><creator>Corrêa, Jôice Dias</creator><creator>Calderaro, Débora Cerqueira</creator><creator>Ferreira, Gilda Aparecida</creator><creator>Mendonça, Santuza Maria Souza</creator><creator>Fernandes, Gabriel R</creator><creator>Xiao, E</creator><creator>Teixeira, Antônio Lúcio</creator><creator>Leys, Eugene J</creator><creator>Graves, Dana T</creator><creator>Silva, Tarcília Aparecida</creator><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170320</creationdate><title>Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status</title><author>Corrêa, Jôice Dias ; Calderaro, Débora Cerqueira ; Ferreira, Gilda Aparecida ; Mendonça, Santuza Maria Souza ; Fernandes, Gabriel R ; Xiao, E ; Teixeira, Antônio Lúcio ; Leys, Eugene J ; Graves, Dana T ; Silva, Tarcília Aparecida</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-b0ef8fd7168319e82a3dbad6216c5a8f78c305d8876016968d603acb9e8f875a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Autoimmune diseases</topic><topic>Bacteria - classification</topic><topic>Bacteria - genetics</topic><topic>Bacteria - isolation & purification</topic><topic>Bacteroides - genetics</topic><topic>Dental plaque</topic><topic>Dental Plaque - microbiology</topic><topic>Dysbiosis</topic><topic>Female</topic><topic>Gingiva - microbiology</topic><topic>Gum disease</topic><topic>High-Throughput Nucleotide Sequencing</topic><topic>Humans</topic><topic>Hypothesis testing</topic><topic>Immunology</topic><topic>Inflammatory diseases</topic><topic>Interleukin-17 - immunology</topic><topic>Interleukin-17 - metabolism</topic><topic>Interleukin-33 - immunology</topic><topic>Interleukin-33 - metabolism</topic><topic>Interleukin-6 - immunology</topic><topic>Interleukin-6 - metabolism</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - microbiology</topic><topic>Male</topic><topic>Microbiota</topic><topic>Microbiota - genetics</topic><topic>Middle Aged</topic><topic>Periodontics</topic><topic>Periodontitis - immunology</topic><topic>Periodontitis - microbiology</topic><topic>Rheumatic diseases</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>RNA, Ribosomal, 16S - genetics</topic><topic>Systemic lupus erythematosus</topic><topic>Teeth</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Corrêa, Jôice Dias</creatorcontrib><creatorcontrib>Calderaro, Débora Cerqueira</creatorcontrib><creatorcontrib>Ferreira, Gilda Aparecida</creatorcontrib><creatorcontrib>Mendonça, Santuza Maria Souza</creatorcontrib><creatorcontrib>Fernandes, Gabriel R</creatorcontrib><creatorcontrib>Xiao, E</creatorcontrib><creatorcontrib>Teixeira, Antônio Lúcio</creatorcontrib><creatorcontrib>Leys, Eugene J</creatorcontrib><creatorcontrib>Graves, Dana T</creatorcontrib><creatorcontrib>Silva, Tarcília Aparecida</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Microbiome</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Corrêa, Jôice Dias</au><au>Calderaro, Débora Cerqueira</au><au>Ferreira, Gilda Aparecida</au><au>Mendonça, Santuza Maria Souza</au><au>Fernandes, Gabriel R</au><au>Xiao, E</au><au>Teixeira, Antônio Lúcio</au><au>Leys, Eugene J</au><au>Graves, Dana T</au><au>Silva, Tarcília Aparecida</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status</atitle><jtitle>Microbiome</jtitle><addtitle>Microbiome</addtitle><date>2017-03-20</date><risdate>2017</risdate><volume>5</volume><issue>1</issue><spage>34</spage><epage>34</epage><pages>34-34</pages><artnum>34</artnum><issn>2049-2618</issn><eissn>2049-2618</eissn><abstract>Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to affect the subgingival microbiota and clinical periodontal status. However, this relationship has not been examined in subjects with systemic lupus erythematosus (SLE). The objective of our study was to investigate the influence of SLE on the subgingival microbiota and its connection with periodontal disease and SLE activity.
We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing.
SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis.
SLE is associated with differences in the composition of the microbiota, independently of periodontal status.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>28320468</pmid><doi>10.1186/s40168-017-0252-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; DOAJ Directory of Open Access Journals; PubMed Central Open Access; Springer Nature OA Free Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SpringerLink Journals - AutoHoldings |
subjects | Adult Autoimmune diseases Bacteria - classification Bacteria - genetics Bacteria - isolation & purification Bacteroides - genetics Dental plaque Dental Plaque - microbiology Dysbiosis Female Gingiva - microbiology Gum disease High-Throughput Nucleotide Sequencing Humans Hypothesis testing Immunology Inflammatory diseases Interleukin-17 - immunology Interleukin-17 - metabolism Interleukin-33 - immunology Interleukin-33 - metabolism Interleukin-6 - immunology Interleukin-6 - metabolism Lupus Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - microbiology Male Microbiota Microbiota - genetics Middle Aged Periodontics Periodontitis - immunology Periodontitis - microbiology Rheumatic diseases Rheumatoid arthritis Rheumatology RNA, Ribosomal, 16S - genetics Systemic lupus erythematosus Teeth Young Adult |
title | Subgingival microbiota dysbiosis in systemic lupus erythematosus: association with periodontal status |
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