Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction
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...
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| Veröffentlicht in: | International journal of rheumatic diseases 2016-07, Vol.19 (7), p.685-692 |
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| container_title | International journal of rheumatic diseases |
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| creator | Houssen, Maha E. El-Mahdy, Rasha H. Shahin, Dina A. |
| description | 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 |
| doi_str_mv | 10.1111/1756-185X.12452 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1815693735</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1815693735</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5822-7a342a8cd501805ebe34375ad82719f40fb8e6a2f8dcdf6c55569ed5962c17f13</originalsourceid><addsrcrecordid>eNqNkU1vFCEchydGY1_07M2QePEy7QDDwHprqruabHSTavRGGPhPpGWGLQxr53v4gWU77R68KBfent8vgacoXuHqDOdxjjlrSizYjzNMakaeFMeHk6eHdY2PipMYr6uqwbThz4sjwjChDa6Oi99XEFKPonepdYBG71zp7A2gABq2ow-IvEMKDX4HDrXW9yrcQEBdvohTHKG3Grm0TRFBmMaf0KvRx7wzNoKKgJQe7c6OE1KDmcEygFMjGKRVMNbvVNTJqYDMFLs0ZNwPL4pnnXIRXj7Mp8W35Yevlx_L9ZfVp8uLdamZIKTkitZECW1YhUXFoAVaU86UEYTjRVdXXSugUaQTRpuu0YyxZgGGLRqiMe8wPS3ezr3b4G8TxFH2NmpwTg3gU5RY4JygnLL_QYkQdEF4Rt_8hV77FIb8kHuqJrmQZup8pnTwMQbo5DbY_LuTxJXcu5V7e3JvUt67zYnXD72p7cEc-EeZGWAz8Ms6mP7VJy8268fics7ZLPTukMumZcPzh8rvn1dyc7VZrt5zLJf0D1hWv_Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1812423733</pqid></control><display><type>article</type><title>Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Houssen, Maha E. ; El-Mahdy, Rasha H. ; Shahin, Dina A.</creator><creatorcontrib>Houssen, Maha E. ; El-Mahdy, Rasha H. ; Shahin, Dina A.</creatorcontrib><description>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.</description><identifier>ISSN: 1756-1841</identifier><identifier>EISSN: 1756-185X</identifier><identifier>DOI: 10.1111/1756-185X.12452</identifier><identifier>PMID: 25123610</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adrenal Cortex Hormones - therapeutic use ; Adult ; Antirheumatic Agents - therapeutic use ; Biomarkers - blood ; Case-Control Studies ; Creatinine - blood ; Cross-Sectional Studies ; Diastole ; Down-Regulation ; Echocardiography, Doppler ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Hydroxychloroquine - therapeutic use ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Hypercholesterolemia - blood ; Hypercholesterolemia - etiology ; Lipids - blood ; Lupus Erythematosus, Systemic - blood ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - diagnosis ; Lupus Erythematosus, Systemic - drug therapy ; lupus-related cardiovascular risk factors ; Male ; systemic lupus erythematosus ; TLR2 signaling (sTLR2) ; Toll-Like Receptor 2 - blood ; Uric Acid - blood ; Ventricular Dysfunction, Left - blood ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Left ; Young Adult</subject><ispartof>International journal of rheumatic diseases, 2016-07, Vol.19 (7), p.685-692</ispartof><rights>2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd</rights><rights>2014 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd.</rights><rights>International Journal of Rheumatic Diseases © 2016 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5822-7a342a8cd501805ebe34375ad82719f40fb8e6a2f8dcdf6c55569ed5962c17f13</citedby><cites>FETCH-LOGICAL-c5822-7a342a8cd501805ebe34375ad82719f40fb8e6a2f8dcdf6c55569ed5962c17f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1756-185X.12452$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1756-185X.12452$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25123610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Houssen, Maha E.</creatorcontrib><creatorcontrib>El-Mahdy, Rasha H.</creatorcontrib><creatorcontrib>Shahin, Dina A.</creatorcontrib><title>Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction</title><title>International journal of rheumatic diseases</title><addtitle>Int J Rheum Dis</addtitle><description>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.</description><subject>Adrenal Cortex Hormones - therapeutic use</subject><subject>Adult</subject><subject>Antirheumatic Agents - therapeutic use</subject><subject>Biomarkers - blood</subject><subject>Case-Control Studies</subject><subject>Creatinine - blood</subject><subject>Cross-Sectional Studies</subject><subject>Diastole</subject><subject>Down-Regulation</subject><subject>Echocardiography, Doppler</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Humans</subject><subject>Hydroxychloroquine - therapeutic use</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Hypercholesterolemia - blood</subject><subject>Hypercholesterolemia - etiology</subject><subject>Lipids - blood</subject><subject>Lupus Erythematosus, Systemic - blood</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - diagnosis</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>lupus-related cardiovascular risk factors</subject><subject>Male</subject><subject>systemic lupus erythematosus</subject><subject>TLR2 signaling (sTLR2)</subject><subject>Toll-Like Receptor 2 - blood</subject><subject>Uric Acid - blood</subject><subject>Ventricular Dysfunction, Left - blood</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Function, Left</subject><subject>Young Adult</subject><issn>1756-1841</issn><issn>1756-185X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1vFCEchydGY1_07M2QePEy7QDDwHprqruabHSTavRGGPhPpGWGLQxr53v4gWU77R68KBfent8vgacoXuHqDOdxjjlrSizYjzNMakaeFMeHk6eHdY2PipMYr6uqwbThz4sjwjChDa6Oi99XEFKPonepdYBG71zp7A2gABq2ow-IvEMKDX4HDrXW9yrcQEBdvohTHKG3Grm0TRFBmMaf0KvRx7wzNoKKgJQe7c6OE1KDmcEygFMjGKRVMNbvVNTJqYDMFLs0ZNwPL4pnnXIRXj7Mp8W35Yevlx_L9ZfVp8uLdamZIKTkitZECW1YhUXFoAVaU86UEYTjRVdXXSugUaQTRpuu0YyxZgGGLRqiMe8wPS3ezr3b4G8TxFH2NmpwTg3gU5RY4JygnLL_QYkQdEF4Rt_8hV77FIb8kHuqJrmQZup8pnTwMQbo5DbY_LuTxJXcu5V7e3JvUt67zYnXD72p7cEc-EeZGWAz8Ms6mP7VJy8268fics7ZLPTukMumZcPzh8rvn1dyc7VZrt5zLJf0D1hWv_Q</recordid><startdate>201607</startdate><enddate>201607</enddate><creator>Houssen, Maha E.</creator><creator>El-Mahdy, Rasha H.</creator><creator>Shahin, Dina A.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201607</creationdate><title>Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction</title><author>Houssen, Maha E. ; El-Mahdy, Rasha H. ; Shahin, Dina A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5822-7a342a8cd501805ebe34375ad82719f40fb8e6a2f8dcdf6c55569ed5962c17f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adrenal Cortex Hormones - therapeutic use</topic><topic>Adult</topic><topic>Antirheumatic Agents - therapeutic use</topic><topic>Biomarkers - blood</topic><topic>Case-Control Studies</topic><topic>Creatinine - blood</topic><topic>Cross-Sectional Studies</topic><topic>Diastole</topic><topic>Down-Regulation</topic><topic>Echocardiography, Doppler</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Humans</topic><topic>Hydroxychloroquine - therapeutic use</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Hypercholesterolemia - blood</topic><topic>Hypercholesterolemia - etiology</topic><topic>Lipids - blood</topic><topic>Lupus Erythematosus, Systemic - blood</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - diagnosis</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>lupus-related cardiovascular risk factors</topic><topic>Male</topic><topic>systemic lupus erythematosus</topic><topic>TLR2 signaling (sTLR2)</topic><topic>Toll-Like Receptor 2 - blood</topic><topic>Uric Acid - blood</topic><topic>Ventricular Dysfunction, Left - blood</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Function, Left</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Houssen, Maha E.</creatorcontrib><creatorcontrib>El-Mahdy, Rasha H.</creatorcontrib><creatorcontrib>Shahin, Dina A.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Houssen, Maha E.</au><au>El-Mahdy, Rasha H.</au><au>Shahin, Dina A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction</atitle><jtitle>International journal of rheumatic diseases</jtitle><addtitle>Int J Rheum Dis</addtitle><date>2016-07</date><risdate>2016</risdate><volume>19</volume><issue>7</issue><spage>685</spage><epage>692</epage><pages>685-692</pages><issn>1756-1841</issn><eissn>1756-185X</eissn><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.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25123610</pmid><doi>10.1111/1756-185X.12452</doi><tpages>8</tpages></addata></record> |
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| ispartof | International journal of rheumatic diseases, 2016-07, Vol.19 (7), p.685-692 |
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| subjects | Adrenal Cortex Hormones - therapeutic use Adult Antirheumatic Agents - therapeutic use Biomarkers - blood Case-Control Studies Creatinine - blood Cross-Sectional Studies Diastole Down-Regulation Echocardiography, Doppler Enzyme-Linked Immunosorbent Assay Female Humans Hydroxychloroquine - therapeutic use Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Hypercholesterolemia - blood Hypercholesterolemia - etiology Lipids - blood Lupus Erythematosus, Systemic - blood Lupus Erythematosus, Systemic - complications Lupus Erythematosus, Systemic - diagnosis Lupus Erythematosus, Systemic - drug therapy lupus-related cardiovascular risk factors Male systemic lupus erythematosus TLR2 signaling (sTLR2) Toll-Like Receptor 2 - blood Uric Acid - blood Ventricular Dysfunction, Left - blood Ventricular Dysfunction, Left - diagnostic imaging Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology Ventricular Function, Left Young Adult |
| title | Serum soluble toll-like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus-related cardiovascular dysfunction |
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