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Aim: This study aimed to investigate the associations between single nucleotide polymorphisms (SNPs) of IL-6 (-174G/C), microRNA146a (rs2910164C/G) and MALAT1 (rs619586A/G) and susceptibility to rheumatoid arthritis (RA) in Egyptians. Methods: SNPs were genotyped in 101 RA patients and 104 controls. Expression levels were evaluated either by Enzyme-linked immunosorbent assay (ELISA) for IL-6 or quantitative real-time PCR (qRT-PCR) for miR-146a and MALAT1. Results:IL-6–174 GC (OR = 3.422) genotype, IL-6–174 C allele (OR = 2.565), miR-146a (rs2910164) CG (OR = 2.190) and MALAT1 (rs619586) AA (OR = 4.125) genotypes and A allele (OR = 6.122) could be considered as risk factors for RA. An increase in the expression of IL-6, miR-146a and MALAT1 was detected in RA patients, which was independent of any SNP. Conclusion: SNPs of IL-6, miR-146a and MALAT1were linked to RA predisposition in Egyptians. Plain Language Summary Rheumatoid arthritis (RA) is a chronic joint disorder with overexpression of inflammatory mediators. There is increasing evidence that epigenetic changes could play a prominent role in RA pathogenesis. This study was designated to explore the associations between genetic mutation of inflammatory cytokines (Interleukin (IL-6) and epigenetic modulators (miR-146a and MALAT1) and susceptibility to RA. Increased production of IL-6, miR-146a and MALAT1 is a remarkable event in RA patients. We provide evidence that certain genotypes could be used as risk factors for the disease. Our data suggest that detecting certain mutations is quite important in disease prediction. Special concern has to be directed to those persons harboring definite genotypes to achieve better clinical manipulation of patients at risk. Tweetable Abstract This study demonstrated an elevation in IL-6, miR-146a and MALAT1 in RA patients. Moreover, we found that susceptibility to RA is associated with IL-6 (rs1800795) GC, miR-146a (rs2910164) CG and MALAT1 (rs619586) AA genotypes. Article highlights IL-6 (-174G/C), miR-146a (rs2910164C/G) and MALAT1 (rs619586A/G) SNPs were thought to be associated with RA risk. This study aimed to investigate this association with RA in Egyptians. in 101 RA patients and 104 controls. IL-6 (-174G/C) was genotyped utilizing MS-PCR, miR-146a (rs2910164 C/G) and MALAT1 (rs619586 A/G) was genotyped using RFLP-PCR. Expression levels were evaluated either by ELISA for IL-6 or qRT-PCR for miR-146a and MALAT1. The statistical analysis showed that IL-6–174GC genotype, C allele and miR-146a (rs2910164) CG genotype were significantly increased in patients versus controls (p < 0.01, p < 0.05, p < 0.01; respectively). Patients showed a significant reduction in IL-6–174GG (p < 0.05), miR-146a (rs2910164) CC genotypes (p < 0.05) and MALAT1(rs619586) G allele (p < 0.05) compared with controls. The genotypes of IL-6–174GC, miR-146a rs2910164 CG and MALAT1 rs619586AA could all be considered risk factors for RA. CGA haplotype was significantly increased (p < 0.01) in patients than in healthy ones. A significant elevation of IL-6, miR-146a and MALAT1 expression levels was detected in RA patients (p < 0.001, p < 0.05 and p < 0.001, respectively). miR-146a was positively correlated with MALAT1 (r = 0.326, p < 0.05) in RA patients. [ABSTRACT FROM AUTHOR]

A triggering receptor expressed on myeloid cells-1 (TREM-1) is a member of the immunoglobulin superfamily with an established role in innate and adaptive immune response. We aimed to determine the plasma concentrations and clinical association of sTREM-1 in Systemic Lupus Erythematosus (SLE) patients. Plasma from 79 SLE patients and 35 normal healthy subjects were assayed for sTREM-1 and IL-6 levels using Enzyme Linked Immunosorbant Assay (ELISA). The clinical disease characteristics and serological data were prospectively assessed. Disease activity was scored using the SLE disease activity index. We detected significantly higher levels of sTREM-1 in plasma of SLE patients than the healthy control group. We also detected high sTREM-1 levels in subgroups of patients with neuropsychiatric manifestations (NPLE) and patients with the total high disease activity and NPLE activity. In addition, sTREM-l levels were significantly correlated with parameters of disease activity, i.e. SLEDAI score, IL-6, hypoalbuminemia. On the other hand, we did not find significant differences in sTREM-1 levels in relation to age, disease duration, medications, ESR, other organ system involvement, or the presence of anti-dsDNA. Our preliminary data indicated that sTREM-1 levels may be an additional useful marker of disease activity in SLE. It also highlights its importance in patients with NPLE. An additional prospective longitudinal study should be carried out to support these findings. [ABSTRACT FROM PUBLISHER]

There are a limited number of studies that report the polarization of the immune system toward the production of T helper 1 (Th1), Th2, or Th17-type cytokines in patients with Behçet's disease (BD). Here, we aimed to detect the presence of various cytokines in serum samples of Egyptian BD patients and to determine the correlation between their production levels and clinical manifestations. To that aim, serum levels of IFN-γ, IL-10, IL-6, and IL-17 measured by ELISA were determined in BD patients with active or inactive disease to evaluate their clinical relevance. The results of the present study show significantly elevated levels of IL-17 and IL-6, as well as a reduction in IL-10, and no change in IFN-γ, in sera of BD patients, as compared to the healthy control group. Moreover, IL-6 serum levels were increased in BD patients in active stages of disease and correlated with arthritic manifestations. On the other hand, IL-10 serum levels were significantly decreased in patients with gastrointestinal tract complications. Furthermore, a positive correlation was observed between IL-10 serum levels and ocular manifestations in BD patients, in contrast to those of IL-17, showing no correlation with the different clinical manifestations. Taken together, the magnitude of IL-6 serum levels could be a potential marker for arthritic manifestations and disease activity, whereas those of IFN-γ, IL-10, and IL-17 cannot be considered predictors for different clinical manifestations in patients with BD.