Ali Hussein Hadi Nassar Al-Tamimi; Nadia Heydari; Saeed Mohammadi; Nafiseh Abdolahi; Seyyed Mehdi Jafari
Abstract
Background: Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease that affects multiple organ systems. The resulting inflammation disrupts adipocyte metabolism, thereby altering the levels of adipokines.Objective: To assess e serum levels of Asprosin and CTRP-6 as novel adipokines in SLE ...
Read More
Background: Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease that affects multiple organ systems. The resulting inflammation disrupts adipocyte metabolism, thereby altering the levels of adipokines.Objective: To assess e serum levels of Asprosin and CTRP-6 as novel adipokines in SLE patients compared to controls, and their association with lipid profiles, oxidative stress markers, and clinical parameters.Methods: This case-control study involved 41 SLE patients and 41 healthy controls. Serum CTRP-6 and Asprosin levels were measured using ELISA, while total antioxidant capacity (TAC) and malondialdehyde levels were measured using a colorimetric assay.Results: The mean serum CTRP-6 level was significantly higher in individuals with SLE (1.08±0.32) compared to healthy subjects (0.82 0.21; P<0.001). Similarly, the serum level of Asprosin was elevated in patients with SLE (11.91 ± 3.09) compared to the control group (10.28 ± 2.09; P < 0.001). In contrast, the TAC level was lower in subjects with SLE than in healthy controls (0.18±0.23, 0.19 0.51 respectively; p<0.001). Additionally, the serum level of Asprosin was significantly reduced in SLE patients with nephritis (10.17 ± 3.55) compared to those without nephritis (12.4 ± 2.75; p = 0.005). Conclusion: Elevated levels of Asprosin and CTRP-6 suggest a potential role for these adipokines in SLE pathogenesis. Moreover, the presence of nephritis in SLE patients was associated with reduced plasma levels of Asprosin.
Yousef Khanjari; Morteza Oladnabi; Nafiseh Abdollahi; Ahmad Heidari; Saeed Mohammadi; Alijan Tabarraei
Abstract
Background: Programmed cell death protein 1 (PD-1) is a negative costimulatory molecule with immunomodulatory properties. Recently, PD-1 gene defects have attracted attention in the pathogenesis of SLE. Objective: Here, we assessed the association of PD-1 gene polymorphisms in intron 4 and haplotypes ...
Read More
Background: Programmed cell death protein 1 (PD-1) is a negative costimulatory molecule with immunomodulatory properties. Recently, PD-1 gene defects have attracted attention in the pathogenesis of SLE. Objective: Here, we assessed the association of PD-1 gene polymorphisms in intron 4 and haplotypes with the susceptibility to SLE. Method: Seventy-six SLE patients and 159 healthy controls were included. We screened the polymorphisms by amplifying the intron 4 of the PD-1 gene with the specific primers followed by sequencing. Results: Two distinct SNPs were identified (rs6705653 and rs41386439) within the intron 4 of the PD-1 gene. The AA genotype of +7499 (G/A) SNP was associated with the higher risk of SLE [OR=3.31, 95% CI (1.25-8.76), p-value=0.045], while A allele was identified as a risk allele [OR=1.75, 95% CI (1.10-2.76), p-value=0.015]. However, no significant association was observed between the allele and the genotype frequencies of +7209 (C/T) polymorphic region of the PD-1 gene and susceptibility to SLE. Haplotype analysis showed the significantly higher presence of H2 haplotype (AC; +7499/+7209) [OR=1.70, 95% CI (1.24-2.33), p-value=0.0012] in SLE patients. Conclusion: To the best of our knowledge, this is the first report of the significant association of PD-1 +7499 (G/A) SNP with the SLE susceptibility and the first detection of both polymorphic loci in a population from Iran. However, more investigations are necessary to confirm these findings.
