Abstract. The aim of the present study was to evaluate the association between the levels of lipids and B-type natriuretic peptide (BNP) in systemic lupus erythematosus (SLE) patients with heart failure (HF). A total of 46 patients with active SLE and 40 healthy, age-matched control subjects were studied. BNP was measured by an immunofluorescence assay in fresh plasma. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, apolipoprotein (Apo) B, ApoA-I and lipoprotein(a) were assessed. Compared with the control subjects, HDL-C and ApoA-I levels were considerably decreased and TG level increased markedly from SLE patients. The average concentration of HDL-C and ApoA-I in the SLE group with HF was significantly reduced compared to those patients without HF. The results showed that the levels of HDL-C and ApoA-I in SLE patients were negatively correlated with BNP. Disease activity was associated with the TC and TG levels. The present data indicated the presence of a cardiovascular (CV) risk in active SLE with high disease activity, which was demonstrated by the high frequency of dyslipidemia and higher BNP concentrations. Therefore, dyslipoproteinemia may underlie some of the increased risk for CV disease and HF in patients with SLE.
Abstract. The tumor necrosis factor α-induced protein-3 (TNFAIP3) gene functions in negative immunoregulation and its single-nucleotide polymorphisms (SNPs) are associated with rheumatoid arthritis (RA) disease. However, its expression level in immune cells from RA patients remains unclear. The aim of the present study was to investigate whether the expression of TNFAIP3 is changed in patients with RA. Reverse transcription-quantitative polymerase chain reaction analysis was used to determine TNFAIP3 mRNA expression in peripheral blood mononuclear cells (PBMCs) from patients with RA and healthy controls. TNFAIP3 expression was decreased in RA patients compared with the healthy controls. The expression level of the TNFAIP3 gene negatively correlated with the RA score, anti-cyclic citrullinated peptide (CCP) antibody levels and C-reactive protein levels. Furthermore, RA patients with positive results of anti-CCP antibodies had a lower expression of TNFAIP3 than those without anti-CCP antibodies. In conclusion, the present results suggest that the insufficient expression of the TNFAIP3 gene in PBMCs may correlate with the diagnosis of RA. IntroductionRheumatoid arthritis (RA) is a common chronic inflammatory disease that predominantly affects the small joints of the hands and feet (1). The propagation of inflammation is characterized by migration of mononuclear cells into the local inflammatory sites, leading to the hyperplasia of fibroblast-like synoviocytes (FLSs) primarily due to resistance to apoptosis and damage to cartilage and bone (2). The chronic inflammation is attributed to breakdown of immune homostasis, which results in activation of immune cells and elevation of pro-inflammatory cytokines (3). The immune activation leads to deposition of immune complexes and mononuclear cell infiltration into susceptible organs, while the pro-inflammatory cytokines are responsible for maintenance of the immune activation (4). The major mediators of chronic inflammation in RA include tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, IL-8 and prostaglandin E2 (5). Induction of pro-inflammatory mediators requires activation of the nuclear factor (NF)-κB inducing kinase-or inhibitor of NF-κB (IκB) kinase-mediated NF-κB signal transduction pathways (6,7). The transcription factor NF-κB has been well recognized as a key regulator of inflammation in RA (8-10).TNF-α-induced protein-3 (TNFAIP3) is an important negative immunoregulatory gene. TNFAIP3 is a dual ubiquitin-editing enzyme, whose expression is induced by a large number of stimuli in a wide variety of cells (11). Evidence from animal models indicates that TNFAIP3 is a plausible candidate gene in RA susceptibility (11). In TNFAIP3 knockout mice, its deficiency leads to death shortly following birth by severe inflammation and tissue damage in multiple organs (12,13). In immune cells, overexpression of TNFAIP3 can terminate NF-κB signaling transduced from TNF receptors, toll-like receptors, nucleotide-binding oligomerization domain containing 2 receptors or T ...
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