Pentraxins are a group of evolutionarily conserved ancient proteins. Depending on their structure, pentraxins are divided into short and long pentraxin families. Pentraxin 3 (PTX3) is the prototype of the long pentraxin group. PTX3 synthesis is stimulated by a variety of molecules involved in the inflammatory process. The inflammatory mediator is typically produced at inflammatory sites; however, it can also be released at the sites remote from the original inflammatory insult. Although mainly expressed by vascular endothelium and smooth muscle cells, PTX3 is also synthesized by myeloid dendritic cells, mononuclear macrophages/phagocytes, vascular endothelial and smooth muscle cells, fibroblasts, adipocytes, cumulus oophorus cells mesangial cells, synovial cells and chondrocytes. PTX3 binds to several ligands including complement component C1q, factor H, ficolin-1 (M-ficolin), mannose-binding lectin, fibroblast growth factor 2, P-selectin, matrix protein TSG6 and Klebsiella pneumoniae; it is also known to play a role in humoral innate immunity as well as in degenerated and apoptotic cells clearance. PTX3 acts as a modulator of inflammatory processes, modifies angiogenesis and atherosclerotic lesion development, and participates in extracellular matrix formation. Due to the fact of PTX3 being primarily produced and released by vascular wall cells, it might be used as a sensitive and independent inflammatory marker.

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease, where vascular lesions are one of the typical symptoms. The pathological process often involves skin vessels, renal glomeruli, the cardiovascular system, brain, lung alveoli, and gastrointestinal tract vessels. This review presents possible adverse mechanisms underlying the cause and effect relationship of various factors causing vascular lesions in SLE patients. The generally accepted hypothesis links vascular damage in SLE with the deposition of immune complexes in the vascular endothelium. The anti-endothelial cell antibodies (AECA), antiphospholipid antibodies and anti-double stranded DNA antibodies present in SLE, that directly or indirectly affect endothelial cells, causing inflammatory damage to the vessel wall, and their role, have been discussed. It has been stressed that although the suggested role of AECA in vasculitis pathogenesis has not been fully established, evidence, however, has demonstrated that AECA is a factor causing endothelial damage in SLE patients. On the other hand, issues concerning cellular adhesion molecules which enable leukocyte adhesion and rolling along the endothelial cell surface, and their extravascular migration, focus on the role they may be playing in SLE patients with vasculitis. A potential role of soluble forms of adhesion molecules, pentraxin 3, medications, infections in the pathogenesis of this disease has also been shown. Special attention has been given to the role of type 3 hepatitis virus in vascular damage in SLE.

The objective of this study was to determine the effect of quinagolide (Norprolac) on serum level of cytokines in systemic lupus erythematosus (SLE) patients. In 20 SLE patients treated with a low dose of quinagolide, and in 17 healthy persons who constituted the control group, concentration of serum prolactin (PRL), interleukins (ILs), soluble tumor necrosis factor receptors (sTNF Rs) preceded by calculation of disease activity index (SLEDAI) were tested at entry and then after 3 months in 16 patients and after 6 months in 11 patients who completed the study. Serum PRL level was higher (though insignificantly) in the SLE group than in the controls and decreased significantly after 6 months of therapy. A raised SLEDAI score at entry was significantly reduced during therapy but a weak correlation with PRL level was revealed. A significant increase in IL-6 level in SLE group as compared to controls was observed (respectively 14.57±13.25 and 5.04± 3.35 pg =ml) as well as a significantly decreased level after 6 months of treatment (4.30±2.51 pg =ml). There was a significant difference between sTNF RI concentration before and after 3 months of quinagolide treatment (respectively 1140.83 312.08 and 1454.58±465.54 pg =ml). After 6 months of treatment a statistically significant correlation between concentration of PRL and level of IL-6 and a negative correlation between PRL and sTNF RI was revealed. Quinagolide treatment may have a role in the management of SLE patients. Lupus (2001) 10, 424–430.