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Abstract Number: 887

Atherosclerosis and Cardiovascular Disease In Systemic Lupus Eryhematosus Are Related To An Inflammatory/Oxidative Status Linked To The Autoimmune Condition and The Clinical Activity Of The Disease. Effect Of Statins Treatment

Chary Lopez-Pedrera1, Patricia Ruiz-Limon1, Carlos Perez-Sanchez1, Mª Angeles Aguirre2, Nuria Barbarroja1, Tomás Cerdó-Ráez3, Maria Laura Bertolaccini4, Munther A. Khamashta5, Antonio Rodriguez-Ariza6, Yolanda Almaden7, Husam Khraiwesh8, Jose Antonio Gonzalez-Reyes9, Jose Manuel Villalba10, Eduardo Collantes11 and Mª Jose Cuadrado12, 1Rheumatology Unit, IMIBIC-Reina Sofia University Hospital, Cordoba, Spain, 2Rheumatology, IMIBIC-Reina Sofia Hospital, Cordoba, Spain, 3Imibic, Córdoba, Spain, 4Lupus Research Unit, The Rayne Institute, Kings College London School of Medicine, London, United Kingdom, 5Lupus Research Unit, The Rayne Institute, St Thomas Hospital, Kings College London School of Medicine, London, United Kingdom, 6Oncology Service and Research Unit, IMIBIC-Reina Sofia Hospital, Cordoba, Spain, 7Imibic, Códoba, Spain, 8UCO, Córdoba, Spain, 9Cell Biology, Physiology and Immunology, University of Cordoba, Cordoba, Spain, 10Cell Biology, Physiology and Immunology, University of Cordoba, Agrifood Campus of International Excelence (ciA3), Cordoba, Spain, 11Rheumatology, Hospital Reina Sofia, Cordoba, Spain, 12Lupus Research Unit, The Rayne Institute, London, United Kingdom

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Atherosclerosis, Cardiovascular disease, Inflammation, statins and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Human Etiology and Pathogenesis I

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Atherosclerosis (AT) and cardiovascular disease (CVD) are enhanced systemic lupus erythematosus (SLE). Although there is evidence that statins have anti-inflammatory properties, their mechanism of action remains incompletely understood. Aims: i) To determine if the proinflammatory SLE profile is related to their oxidative status, and associated to the autoimmune condition and the clinical disease activity; ii) to test the anti-inflammatory effectiveness of fluvastatin. 

Methods: The study was conducted in 85 SLE patients and 62 healthy donors. Flow cytometry, ELISA and enzymatic assays were used to evaluate markers of inflammation and oxidative stress. Carotid-intimate media thickness (CIMT) was used as surrogate marker of AT. Microarray expression profiling was used in paired samples of SLE monocytes from 27 patients before and after of fluvastatin treatment. 

Results:

Increased TF and PAR2 levels were found in monocytes from SLE patients, which also displayed higher plasma levels of VEGF, IL-2, -6, -8, -17, -23, MCP-1, MIP1α and tPA. SLE monocytes displayed an altered mitochondrial membrane potential (MMP) and increased levels of peroxides, peroxynitrites, and antioxidant enzymes. Correlation and association studies demonstrated the existence of an interplay among parameters related to autoimmunity, oxidative stress and inflammation in the development of the disease and on the increased risk of athero-thrombosis in SLE patients. Real time RT-PCR showed that monocytes were major players in the altered expression of the above mentioned proinflammatory parameters.

The in vivo treatment of SLE patients with fluvastatin for one month led to a significant reduction in the activity of the disease and the levels of anti-dsDNA. Analysis of blood cells and serum showed that one month of fluvastatin treatment effectively attenuated SLEDAI and the lipid levels, and reduced the oxidative status and the vascular inflammation. Array studies on monocytes demonstrated that a total of 799 genes displayed significant changes in expression after 1 month of fluvastatin treatment. Many new target genes and pathways modulated by fluvastatin were uncovered. IPA analysis revealed a network of these genes involved in cholesterol and lipid metabolism, inflammation, oxidative stress and mitochondrial activity. Electron microscopy analysis of mitochondria in monocytes from fluvastatin treated SLE patients showed a significant increase in the number of mitochondria in that cells, pointing at an induced process of mitochondrial biogenesis. The increased expression of a set of genes involved in those processes (i.e. PGC1a, PPAR1a, NRF, Sirt-1) confirmed that hypothesis.

Conclusion:

i) Several mediators of autoimmunity, inflammation, and endothelial dysfunction orchestrate in conjunction the pathophysiology of atherothrombosis in SLE ii) A redox-sensitive pathway seems to play a key role in the elicitation of that pathological processes. iii) Fluvastatin has significant anti-inflammatory effects on SLE monocytes, which may partly explain the beneficial pleiotropic effects of statins on cardiovascular disease in the setting of SLE.


Disclosure:

C. Lopez-Pedrera,
None;

P. Ruiz-Limon,
None;

C. Perez-Sanchez,
None;

M. A. Aguirre,
None;

N. Barbarroja,
None;

T. Cerdó-Ráez,
None;

M. L. Bertolaccini,
None;

M. A. Khamashta,
None;

A. Rodriguez-Ariza,
None;

Y. Almaden,
None;

H. Khraiwesh,
None;

J. A. Gonzalez-Reyes,
None;

J. M. Villalba,
None;

E. Collantes,
None;

M. J. Cuadrado,
None.

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