Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction
Identifieur interne : 000131 ( Istex/Corpus ); précédent : 000130; suivant : 000132Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction
Auteurs : Maha E. Houssen ; Rasha H. El-Mahdy ; Dina A. ShahinSource :
- International Journal of Rheumatic Diseases [ 1756-1841 ] ; 2016-07.
Abstract
Aim: To assess the serum levels of soluble toll‐like receptor (sTLR2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between sTLR2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum sTLR2 levels. Methods: Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (sTLR2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected. Results: Mean serum levels of sTLR2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; P < 0.0001). sTLR2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. sTLR2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids. Conclusion: Serum sTLR2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. Statins, corticosteroids and chloroquine increase sTLR2 levels.
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DOI: 10.1111/1756-185X.12452
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El-Mahdy</name><affiliation><mods:affiliation>Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Shahin, Dina A" sort="Shahin, Dina A" uniqKey="Shahin D" first="Dina A." last="Shahin">Dina A. 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Houssen</name><affiliation><mods:affiliation>Biochemistry Department, Faculty of Pharmacy, Damanhour University, Damanhour, Egypt</mods:affiliation></affiliation><affiliation><mods:affiliation>: Dr Maha E. Houssen, Associate Professor of Biochemistry, Faculty of Pharmacy, Damanhour University, Egypt.Email:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mahahoussen@yahoo.com</mods:affiliation></affiliation></author><author><name sortKey="El Ahdy, Rasha H" sort="El Ahdy, Rasha H" uniqKey="El Ahdy R" first="Rasha H." last="El-Mahdy">Rasha H. El-Mahdy</name><affiliation><mods:affiliation>Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</mods:affiliation></affiliation></author><author><name sortKey="Shahin, Dina A" sort="Shahin, Dina A" uniqKey="Shahin D" first="Dina A." last="Shahin">Dina A. Shahin</name><affiliation><mods:affiliation>Internal Medicine Department, Rheumatology and Immunology Unit, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">International Journal of Rheumatic Diseases</title><title level="j" type="alt">INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES</title><idno type="ISSN">1756-1841</idno><idno type="eISSN">1756-185X</idno><imprint><biblScope unit="vol">19</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="685">685</biblScope><biblScope unit="page" to="692">692</biblScope><biblScope unit="page-count">8</biblScope><date type="published" when="2016-07">2016-07</date></imprint><idno type="ISSN">1756-1841</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1756-1841</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Aim: To assess the serum levels of soluble toll‐like receptor (sTLR2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between sTLR2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum sTLR2 levels. Methods: Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (sTLR2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected. Results: Mean serum levels of sTLR2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; P < 0.0001). sTLR2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. sTLR2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids. Conclusion: Serum sTLR2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. 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Houssen</name><affiliations><json:string>Biochemistry Department, Faculty of Pharmacy, Damanhour University, Damanhour, Egypt</json:string><json:string>: Dr Maha E. Houssen, Associate Professor of Biochemistry, Faculty of Pharmacy, Damanhour University, Egypt.Email:</json:string><json:string>E-mail: mahahoussen@yahoo.com</json:string></affiliations></json:item><json:item><name>Rasha H. El‐Mahdy</name><affiliations><json:string>Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</json:string></affiliations></json:item><json:item><name>Dina A. Shahin</name><affiliations><json:string>Internal Medicine Department, Rheumatology and Immunology Unit, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>lupus‐related cardiovascular risk factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>systemic lupus erythematosus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TLR2 signaling (sTLR2)</value></json:item></subject><articleId><json:string>APL12452</json:string></articleId><arkIstex>ark:/67375/WNG-PSPFGD71-F</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Aim: To assess the serum levels of soluble toll‐like receptor (sTLR2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between sTLR2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum sTLR2 levels. Methods: Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (sTLR2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected. Results: Mean serum levels of sTLR2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; P > 0.0001). sTLR2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. sTLR2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids. Conclusion: Serum sTLR2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="apl12452-abs-0001"><head>Abstract</head><head>Aim</head><p>To assess the serum levels of soluble toll‐like receptor (<hi rend="fc">sTLR</hi>2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between <hi rend="fc">sTLR</hi>2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum <hi rend="fc">sTLR</hi>2 levels.</p><head>Methods</head><p>Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (<hi rend="fc">sTLR</hi>2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected.</p><head>Results</head><p>Mean serum levels of <hi rend="fc">sTLR</hi>2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; <hi rend="italic">P </hi><<hi rend="italic"> </hi>0.0001). <hi rend="fc">sTLR</hi>2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. <hi rend="fc">sTLR</hi>2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids.</p><head>Conclusion</head><p>Serum <hi rend="fc">sTLR</hi>2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. Statins, corticosteroids and chloroquine increase <hi rend="fc">sTLR</hi>2 levels.</p></abstract><textClass><keywords><term xml:id="apl12452-kwd-0001">lupus‐related cardiovascular risk factors</term><term xml:id="apl12452-kwd-0002">systemic lupus erythematosus</term><term xml:id="apl12452-kwd-0003">TLR2 signaling (<hi rend="fc">sTLR</hi>2)</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><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-PSPFGD71-F/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="apl12452" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1756-185X</doi><issn type="print">1756-1841</issn><issn type="electronic">1756-185X</issn><idGroup><id type="product" value="APL"></id></idGroup><titleGroup><title sort="INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES" type="main">International Journal of Rheumatic Diseases</title><title type="short">Int J Rheum Dis</title></titleGroup></publicationMeta><publicationMeta level="part" position="70"><doi origin="wiley">10.1111/apl.2016.19.issue-7</doi><copyright ownership="joint"><i>International Journal of Rheumatic Diseases</i> © 2016 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd</copyright><numberingGroup><numbering type="journalVolume" number="19">19</numbering><numbering type="journalIssue">7</numbering></numberingGroup><coverDate startDate="2016-07">July 2016</coverDate></publicationMeta><publicationMeta level="unit" position="100" status="forIssue" type="article"><doi>10.1111/1756-185X.12452</doi><idGroup><id type="unit" value="APL12452"></id></idGroup><countGroup><count number="8" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">© 2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd</copyright><eventGroup><event agent="SPS" date="2014-08-01" type="xmlCreated"></event><event type="firstOnline" date="2014-08-14"></event><event type="publishedOnlineEarlyUnpaginated" date="2014-08-14"></event><event type="publishedOnlineFinalForm" date="2016-08-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:5.0.6 mode:FullText" date="2017-02-09"></event></eventGroup><numberingGroup><numbering type="pageFirst">685</numbering><numbering type="pageLast">692</numbering></numberingGroup><correspondenceTo><lineatedText><line><i>Correspondence</i>: Dr Maha E. Houssen, Associate Professor of Biochemistry, Faculty of Pharmacy, Damanhour University, Egypt.</line><line>Email: <email>mahahoussen@yahoo.com</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:APL.APL12452.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction</title><title type="shortAuthors">M. E. Houssen <i>et al</i>.</title></titleGroup><creators><creator affiliationRef="#apl12452-aff-0001" corresponding="yes" creatorRole="author" xml:id="apl12452-cr-0001"><personName><givenNames>Maha E.</givenNames> <familyName>Houssen</familyName></personName></creator><creator affiliationRef="#apl12452-aff-0002" creatorRole="author" xml:id="apl12452-cr-0002"><personName><givenNames>Rasha H.</givenNames> <familyName>El‐Mahdy</familyName></personName></creator><creator affiliationRef="#apl12452-aff-0003" creatorRole="author" xml:id="apl12452-cr-0003"><personName><givenNames>Dina A.</givenNames> <familyName>Shahin</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="EG" type="organization" xml:id="apl12452-aff-0001"><orgDiv>Biochemistry Department</orgDiv> <orgName>Faculty of Pharmacy</orgName> <orgName>Damanhour University</orgName> <address><city>Damanhour</city> <country>Egypt</country></address></affiliation><affiliation countryCode="EG" type="organization" xml:id="apl12452-aff-0002"><orgDiv>Medical Microbiology and Immunology Department</orgDiv> <orgName>Faculty of Medicine</orgName> <orgName>Mansoura University</orgName> <address><city>Mansoura</city> <countryPart>Dakahlia</countryPart> <country>Egypt</country></address></affiliation><affiliation countryCode="EG" type="organization" xml:id="apl12452-aff-0003"><orgDiv>Internal Medicine Department</orgDiv> <orgDiv>Rheumatology and Immunology Unit</orgDiv> <orgName>Faculty of Medicine</orgName> <orgName>Mansoura University</orgName> <address><city>Mansoura</city> <countryPart>Dakahlia</countryPart> <country>Egypt</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="apl12452-kwd-0001">lupus‐related cardiovascular risk factors</keyword><keyword xml:id="apl12452-kwd-0002">systemic lupus erythematosus</keyword><keyword xml:id="apl12452-kwd-0003">TLR2 signaling (<fc>sTLR</fc>2)</keyword></keywordGroup><abstractGroup><abstract type="main" xml:id="apl12452-abs-0001"><title type="main">Abstract</title><section xml:id="apl12452-sec-0001"><title type="main">Aim</title><p>To assess the serum levels of soluble toll‐like receptor (<fc>sTLR</fc>2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between <fc>sTLR</fc>2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum <fc>sTLR</fc>2 levels.</p></section><section xml:id="apl12452-sec-0002"><title type="main">Methods</title><p>Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (<fc>sTLR</fc>2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected.</p></section><section xml:id="apl12452-sec-0003"><title type="main">Results</title><p>Mean serum levels of <fc>sTLR</fc>2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; <i>P </i><<i> </i>0.0001). <fc>sTLR</fc>2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. <fc>sTLR</fc>2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids.</p></section><section xml:id="apl12452-sec-0004"><title type="main">Conclusion</title><p>Serum <fc>sTLR</fc>2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. Statins, corticosteroids and chloroquine increase <fc>sTLR</fc>2 levels.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction</title></titleInfo><name type="personal"><namePart type="given">Maha E.</namePart><namePart type="family">Houssen</namePart><affiliation>Biochemistry Department, Faculty of Pharmacy, Damanhour University, Damanhour, Egypt</affiliation><affiliation>: Dr Maha E. Houssen, Associate Professor of Biochemistry, Faculty of Pharmacy, Damanhour University, Egypt.Email:</affiliation><affiliation>E-mail: mahahoussen@yahoo.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rasha H.</namePart><namePart type="family">El‐Mahdy</namePart><affiliation>Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dina A.</namePart><namePart type="family">Shahin</namePart><affiliation>Internal Medicine Department, Rheumatology and Immunology Unit, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura, Egypt</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">2016-07</dateIssued><dateCreated encoding="w3cdtf">2014-08-01</dateCreated><copyrightDate encoding="w3cdtf">2016</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Aim: To assess the serum levels of soluble toll‐like receptor (sTLR2) as an endogenous negative regulator of TLR2 signaling in systemic lupus erythematosus (SLE) patients, to investigate the correlation between sTLR2 and SLE disease activity index (SELDAI), SLE‐related cardiovascular risk factors and ventricular dysfunction and to evaluate the effect of different therapeutic regimens on serum sTLR2 levels. Methods: Ninety‐six SLE patients, along with 30 healthy controls, were enrolled in the study. Echocardiography measurements were performed. Serum levels of (sTLR2) were measured using enzyme‐linked immunosorbent assay (ELISA). Serum lipid profiles, uric acid and creatinine were also detected. Results: Mean serum levels of sTLR2 in SLE patients was 3.98 ± 4.4 ng/mL, which was significantly decreased as compared with that of the control group (11.3 ± 4.9 ng/mL; P < 0.0001). sTLR2 was negatively correlated with SELDAI, low‐density lipoprotein (LDL) and left ventricular diastolic dysfunction. sTLR2 levels were increased in patients receiving hydroxychloroquine, statins and corticosteroids. Conclusion: Serum sTLR2 can attenuate disease activity and negatively impact left ventricular diastolic dysfunction and hypercholersterelemia in SLE patients. 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