Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis
Identifieur interne : 005B54 ( Istex/Corpus ); précédent : 005B53; suivant : 005B55Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis
Auteurs : V. Swaminathan ; S. Prakasam ; V. Puri ; M. SrinivasanSource :
- Journal of Periodontal Research [ 0022-3484 ] ; 2013-12.
English descriptors
- KwdEn :
- Actinomycetemcomitans, Buccal, Chronic periodontitis, Clin, Clinical attachment loss, Control subjects, Cytokine, Cytokine secretion, Epithelial, Epithelial cells, Epithelium, Exfoliated, Exfoliation, Gingivalis, Healthy controls, Healthy subjects, Host response, Human saliva, John wiley sons, Ligand, Microbial, Microbial products, Molecular patterns, Mrna, Mucosal, Mucosal epithelial cells, Mucosal surfaces, Oral cavity, Oral epithelial cells, Oral mucosa, Oral mucosal epithelial cells, Pathogen, Peptidoglycan, Peptidoglycan recognition proteins, Periodontal, Periodontal disease, Periodontal pathogens, Periodontitis, Periodontol, Periodontopathic bacteria, Pgrp4 mrnas, Porphyromonas gingivalis, Protein peptide, Receptor, Relative quantities, Saliva, Salivary, Salivary epithelial cells, Small proline, Sprr2a, Time point, Tlr2, Tlr2 mrna, Tlr4, Tlr4 mrna, Tlr4 mrnas, Tlrs.
- Teeft :
- Actinomycetemcomitans, Buccal, Chronic periodontitis, Clin, Clinical attachment loss, Control subjects, Cytokine, Cytokine secretion, Epithelial, Epithelial cells, Epithelium, Exfoliated, Exfoliation, Gingivalis, Healthy controls, Healthy subjects, Host response, Human saliva, John wiley sons, Ligand, Microbial, Microbial products, Molecular patterns, Mrna, Mucosal, Mucosal epithelial cells, Mucosal surfaces, Oral cavity, Oral epithelial cells, Oral mucosa, Oral mucosal epithelial cells, Pathogen, Peptidoglycan, Peptidoglycan recognition proteins, Periodontal, Periodontal disease, Periodontal pathogens, Periodontitis, Periodontol, Periodontopathic bacteria, Pgrp4 mrnas, Porphyromonas gingivalis, Protein peptide, Receptor, Relative quantities, Saliva, Salivary, Salivary epithelial cells, Small proline, Sprr2a, Time point, Tlr2, Tlr2 mrna, Tlr4, Tlr4 mrna, Tlr4 mrnas, Tlrs.
Abstract
Chronic periodontitis is initiated by sequential colonization with a broad array of bacteria and is perpetuated by an immune‐inflammatory response to the changing biofilm. Host recognition of microbes is largely mediated by toll‐like receptors (TLRs), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, TLR‐2 and TLR‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional TLRs. In this study we investigated the role of salivary epithelial cell (SEC) TLR‐2 and TLR‐4 in patients with generalized chronic periodontitis.
Url:
DOI: 10.1111/jre.12066
Links to Exploration step
ISTEX:B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2Le document en format XML
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Host recognition of microbes is largely mediated by toll‐like receptors (TLRs), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, TLR‐2 and TLR‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional TLRs. In this study we investigated the role of salivary epithelial cell (SEC) TLR‐2 and TLR‐4 in patients with generalized chronic periodontitis.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>epithelial</json:string><json:string>periodontitis</json:string><json:string>epithelial cells</json:string><json:string>chronic periodontitis</json:string><json:string>periodontal</json:string><json:string>receptor</json:string><json:string>healthy controls</json:string><json:string>periodontol</json:string><json:string>mrna</json:string><json:string>mucosal</json:string><json:string>clin</json:string><json:string>epithelium</json:string><json:string>pathogen</json:string><json:string>gingivalis</json:string><json:string>actinomycetemcomitans</json:string><json:string>peptidoglycan</json:string><json:string>tlr4</json:string><json:string>exfoliation</json:string><json:string>buccal</json:string><json:string>exfoliated</json:string><json:string>tlr2</json:string><json:string>cytokine</json:string><json:string>tlrs</json:string><json:string>oral epithelial cells</json:string><json:string>clinical attachment loss</json:string><json:string>sprr2a</json:string><json:string>salivary</json:string><json:string>ligand</json:string><json:string>periodontal disease</json:string><json:string>periodontal pathogens</json:string><json:string>tlr4 mrna</json:string><json:string>human saliva</json:string><json:string>oral mucosa</json:string><json:string>salivary epithelial cells</json:string><json:string>oral mucosal epithelial cells</json:string><json:string>microbial products</json:string><json:string>healthy subjects</json:string><json:string>john wiley sons</json:string><json:string>porphyromonas gingivalis</json:string><json:string>microbial</json:string><json:string>cytokine secretion</json:string><json:string>control subjects</json:string><json:string>periodontopathic bacteria</json:string><json:string>protein peptide</json:string><json:string>mucosal surfaces</json:string><json:string>pgrp4 mrnas</json:string><json:string>tlr4 mrnas</json:string><json:string>tlr2 mrna</json:string><json:string>host response</json:string><json:string>small proline</json:string><json:string>relative quantities</json:string><json:string>time point</json:string><json:string>oral cavity</json:string><json:string>mucosal epithelial cells</json:string><json:string>molecular patterns</json:string><json:string>peptidoglycan recognition proteins</json:string><json:string>saliva</json:string></teeft></keywords><author><json:item><name>V. Swaminathan</name><affiliations><json:string>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</json:string></affiliations></json:item><json:item><name>S. Prakasam</name><affiliations><json:string>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</json:string></affiliations></json:item><json:item><name>V. Puri</name><affiliations><json:string>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</json:string></affiliations></json:item><json:item><name>M. Srinivasan</name><affiliations><json:string>Oral Pathology, Medicine and Radiology, School of Dentistry, The Indiana University, Purdue University, IN, Indianapolis, USA</json:string><json:string>Mythily Srinivasan, MDS, PhD, Immunology Laboratory, 1121, West Michigan Street, Indianapolis, IN 46202, USATel: +317 278 9686Fax: +317 278 3018e‐mail:</json:string><json:string>E-mail: mysriniv@iupui.edu</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>epithelial cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>periodontitis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>proteoglycan recognition protein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>saliva</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>toll‐like receptors</value></json:item></subject><articleId><json:string>JRE12066</json:string></articleId><arkIstex>ark:/67375/WNG-RKM33JVC-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Chronic periodontitis is initiated by sequential colonization with a broad array of bacteria and is perpetuated by an immune‐inflammatory response to the changing biofilm. Host recognition of microbes is largely mediated by toll‐like receptors (TLRs), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, TLR‐2 and TLR‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional TLRs. In this study we investigated the role of salivary epithelial cell (SEC) TLR‐2 and TLR‐4 in patients with generalized chronic periodontitis.</abstract><qualityIndicators><score>8.248</score><pdfWordCount>5367</pdfWordCount><pdfCharCount>38180</pdfCharCount><pdfVersion>1.7</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>104</abstractWordCount><abstractCharCount>755</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title><pmid><json:string>23679005</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Periodontal Research</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-0765</json:string></doi><issn><json:string>0022-3484</json:string></issn><eissn><json:string>1600-0765</json:string></eissn><publisherId><json:string>JRE</json:string></publisherId><volume>48</volume><issue>6</issue><pages><first>757</first><last>765</last><total>9</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2013-03-13</json:string></date><geogName></geogName><orgName><json:string>Stem Cell Technologies, Vancouver</json:string><json:string>Purdue University</json:string><json:string>CELL Applications, Inc., San Diego</json:string><json:string>Genway Biotech Inc., San Diego</json:string><json:string>Mediatech Inc.</json:string><json:string>The Indiana University</json:string><json:string>Indiana University</json:string><json:string>D Systems, Minneapolis</json:string><json:string>Difco Laboratories, Detroit</json:string><json:string>Santa Cruz Biotechnology Inc.</json:string><json:string>Indiana University Purdue University</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>John Wiley</json:string><json:string>The</json:string><json:string>V. Swaminathan</json:string><json:string>S. Prakasam</json:string><json:string>Review Board</json:string><json:string>M. Srinivasan</json:string><json:string>M. Role</json:string><json:string>S. Published</json:string></persName><placeName><json:string>Valencia</json:string><json:string>Minnesota</json:string><json:string>IN</json:string><json:string>Canada</json:string><json:string>San Jose</json:string><json:string>USA</json:string><json:string>Santa Cruz</json:string><json:string>Puri</json:string><json:string>CA</json:string><json:string>Indianapolis</json:string><json:string>MN</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Uhera et al.</json:string><json:string>Swaminathan et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-RKM33JVC-W</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - dentistry, oral surgery & medicine</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - dentistry</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - Periodontics</json:string></scopus></categories><publicationDate>2013</publicationDate><copyrightDate>2013</copyrightDate><doi><json:string>10.1111/jre.12066</json:string></doi><id>B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Publishing Ltd</publisher><availability><licence>© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</licence></availability><date type="published" when="2013-12"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title><author xml:id="author-0000"><persName><forename type="first">V.</forename><surname>Swaminathan</surname></persName><affiliation><orgName>Department of Periodontics and Allied Health</orgName><orgName>School of Dentistry</orgName><orgName>Indiana University Purdue</orgName><orgName>University at Indianapolis</orgName><address><settlement type="city">Indianapolis</settlement><region>IN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">S.</forename><surname>Prakasam</surname></persName><affiliation><orgName>Department of Periodontics and Allied Health</orgName><orgName>School of Dentistry</orgName><orgName>Indiana University Purdue</orgName><orgName>University at Indianapolis</orgName><address><settlement type="city">Indianapolis</settlement><region>IN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">V.</forename><surname>Puri</surname></persName><affiliation><orgName>Department of Periodontics and Allied Health</orgName><orgName>School of Dentistry</orgName><orgName>Indiana University Purdue</orgName><orgName>University at Indianapolis</orgName><address><settlement type="city">Indianapolis</settlement><region>IN</region><country key="US">USA</country></address></affiliation></author><author xml:id="author-0003" role="corresp"><persName><forename type="first">M.</forename><surname>Srinivasan</surname></persName><affiliation><orgName>Oral Pathology, Medicine and Radiology</orgName><orgName>School of Dentistry</orgName><orgName>The Indiana University, Purdue University</orgName><address><settlement type="city">Indianapolis</settlement><region>IN</region><country key="US">USA</country></address></affiliation><affiliation>Mythily Srinivasan, MDS, PhD, Immunology Laboratory, 1121, West Michigan Street, Indianapolis, IN 46202, USA Tel: +317 278 9686 Fax: +317 278 3018 e‐mail: mysriniv@iupui.edu</affiliation></author><idno type="istex">B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2</idno><idno type="ark">ark:/67375/WNG-RKM33JVC-W</idno><idno type="DOI">10.1111/jre.12066</idno><idno type="unit">JRE12066</idno><idno type="toTypesetVersion">file:JRE.JRE12066.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Periodontal Research</title><title level="j" type="alt">JOURNAL OF PERIODONTAL RESEARCH</title><idno type="pISSN">0022-3484</idno><idno type="eISSN">1600-0765</idno><idno type="book-DOI">10.1111/(ISSN)1600-0765</idno><idno type="book-part-DOI">10.1111/jre.2013.48.issue-6</idno><idno type="product">JRE</idno><imprint><biblScope unit="vol">48</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="757">757</biblScope><biblScope unit="page" to="765">765</biblScope><biblScope unit="page-count">9</biblScope><date type="published" when="2013-12"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract style="main" xml:id="jre12066-abs-0001">
Background and Objective
<p>Chronic periodontitis is initiated by sequential colonization with a broad array of bacteria and is perpetuated by an immune‐inflammatory response to the changing biofilm. Host recognition of microbes is largely mediated by toll‐like receptors (<hi rend="fc">TLRs</hi>), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, <hi rend="fc">TLR</hi>‐2 and <hi rend="fc">TLR</hi>‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional <hi rend="fc">TLR</hi>s. In this study we investigated the role of salivary epithelial cell (<hi rend="fc">SEC</hi>) <hi rend="fc">TLR</hi>‐2 and <hi rend="fc">TLR</hi>‐4 in patients with generalized chronic periodontitis.</p>
Material and Methods
<p>Unstimulated whole saliva (<hi rend="fc">UWS</hi>) was collected from patients with generalized chronic periodontitis and from healthy individuals after obtaining informed consent. Epithelial cells isolated from each <hi rend="fc">UWS</hi> sample were assessed for <hi rend="fc">TLR</hi>‐2, <hi rend="fc">TLR</hi>‐4, peptidoglycan recognition protein (<hi rend="fc">PGRP)</hi>‐3 and <hi rend="fc">PGRP</hi>‐4 by quantitative real‐time PCR. In addition, the <hi rend="fc">SEC</hi>s were stimulated <hi rend="italic">in vitro</hi> with microbial products for up to 24 h. The culture supernatant was assessed for cytokines by <hi rend="fc">ELISA</hi>.</p>
Results
<p>Stimulation with TLR‐2‐ or TLR‐4‐specific ligands induced cytokine secretion with differential kinetics and up‐regulated <hi rend="italic">TLR</hi>2 and <hi rend="italic">TLR4</hi> m<hi rend="fc">RNAs,</hi> respectively, in cultures of SECs from patients with periodontitis. In addition, the SECs from patients with periodontitis exhibited reduced <hi rend="italic">PGRP3</hi> and <hi rend="italic">PGRP4</hi> m<hi rend="fc">RNAs</hi>, the TLR‐responsive genes with antibacterial properties.</p>
Conclusion
<p><hi rend="fc">SECs</hi> derived from the <hi rend="fc">UWS</hi> of patients with chronic periodontitis are phenotypically distinct and could represent potential resources for assessing the epithelial responses to periodontal pathogens in the course of disease progression and persistence.</p></abstract><textClass><keywords><term xml:id="jre12066-kwd-0001">epithelial cells</term><term xml:id="jre12066-kwd-0002">periodontitis</term><term xml:id="jre12066-kwd-0003">proteoglycan recognition protein</term><term xml:id="jre12066-kwd-0004">saliva</term><term xml:id="jre12066-kwd-0005">toll‐like receptors</term></keywords><keywords rend="articleCategory"><term>Original Article</term></keywords><keywords rend="tocHeading1"><term>ORIGINAL ARTICLES</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="jre12066" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0765</doi><issn type="print">0022-3484</issn><issn type="electronic">1600-0765</issn><idGroup><id type="product" value="JRE"></id></idGroup><titleGroup><title sort="JOURNAL OF PERIODONTAL RESEARCH" type="main">Journal of Periodontal Research</title><title type="short">J Periodont Res</title></titleGroup></publicationMeta><publicationMeta level="part" position="12106"><doi origin="wiley">10.1111/jre.2013.48.issue-6</doi><copyright ownership="publisher">Copyright © 2013 John Wiley & Sons A/S</copyright><numberingGroup><numbering type="journalVolume" number="48">48</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="2013-12">December 2013</coverDate></publicationMeta><publicationMeta level="unit" position="110" status="forIssue" type="article"><doi>10.1111/jre.12066</doi><idGroup><id type="unit" value="JRE12066"></id></idGroup><countGroup><count number="9" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><copyright ownership="publisher">© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><eventGroup><event date="2013-01-28" type="manuscriptAccepted"></event><event agent="SPS" date="2013-03-13" type="xmlCreated"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.2.6 mode:FullText" date="2013-11-07"></event><event type="publishedOnlineEarlyUnpaginated" date="2013-05-17"></event><event type="firstOnline" date="2013-05-17"></event><event type="publishedOnlineFinalForm" date="2013-11-07"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-01"></event></eventGroup><numberingGroup><numbering type="pageFirst">757</numbering><numbering type="pageLast">765</numbering></numberingGroup><correspondenceTo><lineatedText><line>Mythily Srinivasan, MDS, PhD, Immunology Laboratory, 1121, West Michigan Street, Indianapolis, IN 46202, USA</line><line>Tel: +317 278 9686</line><line>Fax: +317 278 3018</line><line>e‐mail: <email>mysriniv@iupui.edu</email></line></lineatedText></correspondenceTo><selfCitationGroup><citation type="self" xml:id="jre12066-cit-1001"><author><familyName>Swaminathan</familyName> <givenNames>V</givenNames></author>, <author><familyName>Prakasam</familyName> <givenNames>S</givenNames></author>, <author><familyName>Puri</familyName> <givenNames>V</givenNames></author>, <author><familyName>Srinivasan</familyName> <givenNames>M</givenNames></author>. <articleTitle>Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</articleTitle>. <journalTitle>J Periodont Res</journalTitle> <pubYear year="2013">2013</pubYear>; <vol>48</vol>: <pageFirst>757</pageFirst>–<pageLast>765</pageLast>. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</citation></selfCitationGroup><linkGroup><link type="toTypesetVersion" href="file:JRE.JRE12066.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title><title type="shortAuthors"><i>Swaminathan</i> et al.</title></titleGroup><creators><creator affiliationRef="#jre12066-aff-0001" creatorRole="author" xml:id="jre12066-cr-0001"><personName><givenNames>V.</givenNames> <familyName>Swaminathan</familyName></personName></creator><creator affiliationRef="#jre12066-aff-0001" creatorRole="author" xml:id="jre12066-cr-0002"><personName><givenNames>S.</givenNames> <familyName>Prakasam</familyName></personName></creator><creator affiliationRef="#jre12066-aff-0001" creatorRole="author" xml:id="jre12066-cr-0003"><personName><givenNames>V.</givenNames> <familyName>Puri</familyName></personName></creator><creator affiliationRef="#jre12066-aff-0002" corresponding="yes" creatorRole="author" xml:id="jre12066-cr-0004"><personName><givenNames>M.</givenNames> <familyName>Srinivasan</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="US" type="organization" xml:id="jre12066-aff-0001"><orgDiv>Department of Periodontics and Allied Health</orgDiv> <orgDiv>School of Dentistry</orgDiv> <orgName>Indiana University Purdue</orgName> <orgName>University at Indianapolis</orgName> <address><city>Indianapolis</city> <countryPart>IN</countryPart> <country>USA</country></address></affiliation><affiliation countryCode="US" type="organization" xml:id="jre12066-aff-0002"><orgDiv>Oral Pathology, Medicine and Radiology</orgDiv> <orgDiv>School of Dentistry</orgDiv> <orgName>The Indiana University, Purdue University</orgName> <address><city>Indianapolis</city> <countryPart>IN</countryPart> <country>USA</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="jre12066-kwd-0001">epithelial cells</keyword><keyword xml:id="jre12066-kwd-0002">periodontitis</keyword><keyword xml:id="jre12066-kwd-0003">proteoglycan recognition protein</keyword><keyword xml:id="jre12066-kwd-0004">saliva</keyword><keyword xml:id="jre12066-kwd-0005">toll‐like receptors</keyword></keywordGroup><fundingInfo><fundingAgency>Indiana University of School of Dentistry student research subcommittee</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:id="jre12066-abs-0001"><section xml:id="jre12066-sec-0001"><title type="main">Background and Objective</title><p>Chronic periodontitis is initiated by sequential colonization with a broad array of bacteria and is perpetuated by an immune‐inflammatory response to the changing biofilm. Host recognition of microbes is largely mediated by toll‐like receptors (<fc>TLRs</fc>), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, <fc>TLR</fc>‐2 and <fc>TLR</fc>‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional <fc>TLR</fc>s. In this study we investigated the role of salivary epithelial cell (<fc>SEC</fc>) <fc>TLR</fc>‐2 and <fc>TLR</fc>‐4 in patients with generalized chronic periodontitis.</p></section><section xml:id="jre12066-sec-0002"><title type="main">Material and Methods</title><p>Unstimulated whole saliva (<fc>UWS</fc>) was collected from patients with generalized chronic periodontitis and from healthy individuals after obtaining informed consent. Epithelial cells isolated from each <fc>UWS</fc> sample were assessed for <fc>TLR</fc>‐2, <fc>TLR</fc>‐4, peptidoglycan recognition protein (<fc>PGRP)</fc>‐3 and <fc>PGRP</fc>‐4 by quantitative real‐time PCR. In addition, the <fc>SEC</fc>s were stimulated <i>in vitro</i> with microbial products for up to 24 h. The culture supernatant was assessed for cytokines by <fc>ELISA</fc>.</p></section><section xml:id="jre12066-sec-0003"><title type="main">Results</title><p>Stimulation with TLR‐2‐ or TLR‐4‐specific ligands induced cytokine secretion with differential kinetics and up‐regulated <i>TLR</i>2 and <i>TLR4</i> m<fc>RNAs,</fc> respectively, in cultures of SECs from patients with periodontitis. In addition, the SECs from patients with periodontitis exhibited reduced <i>PGRP3</i> and <i>PGRP4</i> m<fc>RNAs</fc>, the TLR‐responsive genes with antibacterial properties.</p></section><section xml:id="jre12066-sec-0004"><title type="main">Conclusion</title><p><fc>SECs</fc> derived from the <fc>UWS</fc> of patients with chronic periodontitis are phenotypically distinct and could represent potential resources for assessing the epithelial responses to periodontal pathogens in the course of disease progression and persistence.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis</title></titleInfo><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Swaminathan</namePart><affiliation>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Prakasam</namePart><affiliation>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Puri</namePart><affiliation>Department of Periodontics and Allied Health, School of Dentistry, Indiana University Purdue, University at Indianapolis, IN, Indianapolis, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Srinivasan</namePart><affiliation>Oral Pathology, Medicine and Radiology, School of Dentistry, The Indiana University, Purdue University, IN, Indianapolis, USA</affiliation><affiliation>Mythily Srinivasan, MDS, PhD, Immunology Laboratory, 1121, West Michigan Street, Indianapolis, IN 46202, USATel: +317 278 9686Fax: +317 278 3018e‐mail:</affiliation><affiliation>E-mail: mysriniv@iupui.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-12</dateIssued><dateCreated encoding="w3cdtf">2013-03-13</dateCreated><dateValid encoding="w3cdtf">2013-01-28</dateValid><edition>Swaminathan V, Prakasam S, Puri V, Srinivasan M. Role of salivary epithelial toll‐like receptors 2 and 4 in modulating innate immune responses in chronic periodontitis. J Periodont Res 2013; 48: 757–765. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</edition><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Chronic periodontitis is initiated by sequential colonization with a broad array of bacteria and is perpetuated by an immune‐inflammatory response to the changing biofilm. Host recognition of microbes is largely mediated by toll‐like receptors (TLRs), which interact with conserved pathogen‐associated molecular patterns. Based on ligand recognition, TLR‐2 and TLR‐4 interact with most periodontal pathogens. Extracrevicular bacterial reservoirs, such as the oral epithelial cells, contribute to the persistence of periodontitis. Human saliva is a rich source of oral epithelial cells that express functional TLRs. In this study we investigated the role of salivary epithelial cell (SEC) TLR‐2 and TLR‐4 in patients with generalized chronic periodontitis.</abstract><abstract>Unstimulated whole saliva (UWS) was collected from patients with generalized chronic periodontitis and from healthy individuals after obtaining informed consent. Epithelial cells isolated from each UWS sample were assessed for TLR‐2, TLR‐4, peptidoglycan recognition protein (PGRP)‐3 and PGRP‐4 by quantitative real‐time PCR. In addition, the SECs were stimulated in vitro with microbial products for up to 24 h. The culture supernatant was assessed for cytokines by ELISA.</abstract><abstract>Stimulation with TLR‐2‐ or TLR‐4‐specific ligands induced cytokine secretion with differential kinetics and up‐regulated TLR2 and TLR4 mRNAs, respectively, in cultures of SECs from patients with periodontitis. In addition, the SECs from patients with periodontitis exhibited reduced PGRP3 and PGRP4 mRNAs, the TLR‐responsive genes with antibacterial properties.</abstract><abstract>SECs derived from the UWS of patients with chronic periodontitis are phenotypically distinct and could represent potential resources for assessing the epithelial responses to periodontal pathogens in the course of disease progression and persistence.</abstract><note type="funding">Indiana University of School of Dentistry student research subcommittee</note><subject><genre>keywords</genre><topic>epithelial cells</topic><topic>periodontitis</topic><topic>proteoglycan recognition protein</topic><topic>saliva</topic><topic>toll‐like receptors</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Periodontal Research</title></titleInfo><titleInfo type="abbreviated"><title>J Periodont Res</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic></subject><identifier type="ISSN">0022-3484</identifier><identifier type="eISSN">1600-0765</identifier><identifier type="DOI">10.1111/(ISSN)1600-0765</identifier><identifier type="PublisherID">JRE</identifier><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>48</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>757</start><end>765</end><total>9</total></extent></part></relatedItem><identifier type="istex">B7A477E9D3C5D3A05A238FC0D8411B5B27324AE2</identifier><identifier type="ark">ark:/67375/WNG-RKM33JVC-W</identifier><identifier type="DOI">10.1111/jre.12066</identifier><identifier type="ArticleID">JRE12066</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2013 John Wiley & Sons A/S© 2013 John Wiley & Sons A/S. 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