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BioMed Research International
Volume 2015, Article ID 292851, 9 pages
Research Article

Differential Regulation of Proinflammatory Mediators following LPS- and ATP-Induced Activation of Monocytes from Patients with Antiphospholipid Syndrome

1Department of Pathological Physiology, Faculty of Medicine and Dentistry, Palacky University, 775 20 Olomouc, Czech Republic
2Group of Molecular and Cellular Immunology, Institute of Molecular Biology, National Academy of Sciences, 0014 Yerevan, Armenia
3Department of Obstetrics, Institute of Perinatology, Obstetrics and Gynecology, 0078 Yerevan, Armenia
4Laboratory of Macromolecular Complexes, Institute of Molecular Biology, National Academy of Sciences, 0014 Yerevan, Armenia

Received 16 January 2015; Accepted 3 February 2015

Academic Editor: Marija Mostarica-Stojković

Copyright © 2015 Anush Martirosyan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by recurrent thrombosis and pregnancy morbidity in association with the presence of antiphospholipid antibodies. Growing evidence supports the involvement of monocytes in APS pathogenesis. Inflammatory activation of monocytes promotes thrombus formation and other APS complications. However, mechanisms underlying their activation are poorly investigated. We aimed to determine transcriptional activity of monocytes after exposing them to low concentrations of lipopolysaccharide (LPS) and LPS + adenosine triphosphate (ATP) using comparative qRT-PCR. The results showed that LPS significantly increased transcriptional levels of TLR2, IL-23, CCL2, CXCL10, IL-1β, and IL-6 in APS cells, while, in cells from healthy donors, LPS resulted in IL-6 and STAT3 elevated mRNAs. Double stimulation of the cells resulted in decreased mRNA levels of NLRP3 in monocytes isolated from healthy donors and CCL2, IL-1β in APS cells. By contrast, TLR2 mRNAs were elevated in both investigated groups after culture of the cells with LPS + ATP. Thus, the findings indicate increased sensitivity of APS cells to LPS that may contribute to thrombus formation and enhance development or progression of autoimmune processes. Low concentrations of ATP diminish LPS-induced inflammatory state of APS monocytes which might be a potential mechanism which regulates inflammatory state of the cells.