Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction
Identifieur interne : 000D91 ( Main/Exploration ); précédent : 000D90; suivant : 000D92Serum soluble toll‐like receptor 2: a novel biomarker for systemic lupus erythematosus disease activity and lupus‐related cardiovascular dysfunction
Auteurs : Maha E. Houssen [Égypte] ; Rasha H. El-Mahdy [Égypte] ; Dina A. Shahin [Égypte]Source :
- 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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Houssen</name><affiliation wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Biochemistry Department, Faculty of Pharmacy, Damanhour University, Damanhour</wicri:regionArea><wicri:noRegion>Damanhour</wicri:noRegion></affiliation><affiliation></affiliation><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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Medical Microbiology and Immunology Department, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura</wicri:regionArea><wicri:noRegion>Mansoura</wicri:noRegion></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 wicri:level="1"><country xml:lang="fr">Égypte</country><wicri:regionArea>Internal Medicine Department, Rheumatology and Immunology Unit, Faculty of Medicine, Mansoura University, Dakahlia, Mansoura</wicri:regionArea><wicri:noRegion>Mansoura</wicri:noRegion></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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