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Expression and clinical significance of the NEK7-NLRP3 inflammasome signaling pathway in patients with systemic lupus erythematosus.
Background: The aim of the study was to investigate the expression of the NEK7-NLRP3 inflammasome signaling pathway in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE), as well as its clinical significance.
Methods: A total of 38 SLE patients and 33 healthy volunteers were recruited. Real time PCR and western blotting were performed to determine mRNA and protein levels of NEK7 , NLRP3 inflammasome components ( NLRP3 , ASC , and Caspase-1 ), and downstream cytokines ( IL-1b and IL-18 ) in PBMCs from the two groups. ELISA was used to detect serum levels of IL-1b and IL-18 . The same methods were used to detect changes in the above indices in the 25 SLE patients after treatment. Correlations between clinical and laboratory parameters were also analyzed.
Results: Compared to those in healthy controls, levels of NEK7, NLPR3, and ASC were lower in SLE patients; however, Caspase-1 , IL-1b , and IL-18 were expressed at higher levels. mRNA levels of NEK7 , NLRP3 , and ASC were inversely correlated with disease activity, whereas a positive correlation was observed with IL-1b and IL-18 . After treatment, mRNA levels of NEK7 and NLRP3 increased, whereas Caspase-1 , IL-1b , and IL-18 decreased significantly. Compared to those in SLE patients without renal damage, patients with lupus nephritis (LN) exhibited lower mRNA levels of NEK7 , NLRP3 , and ASC but higher levels of Caspase-1 , IL-1b , and IL-18 .
Conclusions: Results indicate that the expression of the NEK7-NLRP3 complex might play a protective role in the pathogenesis of SLE and is inversely correlated with disease activity. A positive effect of NEK7 on NLRP3 was observed, and the low expression of NLRP3 in SLE patients might be related to the low expression of NEK7 . Overexpression of Caspase-1 in SLE patients mediates the maturation and release of IL-1b and IL-18 , and contributes to the pathogenesis of SLE and LN.
Methods: A total of 38 SLE patients and 33 healthy volunteers were recruited. Real time PCR and western blotting were performed to determine mRNA and protein levels of NEK7 , NLRP3 inflammasome components ( NLRP3 , ASC , and Caspase-1 ), and downstream cytokines ( IL-1b and IL-18 ) in PBMCs from the two groups. ELISA was used to detect serum levels of IL-1b and IL-18 . The same methods were used to detect changes in the above indices in the 25 SLE patients after treatment. Correlations between clinical and laboratory parameters were also analyzed.
Results: Compared to those in healthy controls, levels of NEK7, NLPR3, and ASC were lower in SLE patients; however, Caspase-1 , IL-1b , and IL-18 were expressed at higher levels. mRNA levels of NEK7 , NLRP3 , and ASC were inversely correlated with disease activity, whereas a positive correlation was observed with IL-1b and IL-18 . After treatment, mRNA levels of NEK7 and NLRP3 increased, whereas Caspase-1 , IL-1b , and IL-18 decreased significantly. Compared to those in SLE patients without renal damage, patients with lupus nephritis (LN) exhibited lower mRNA levels of NEK7 , NLRP3 , and ASC but higher levels of Caspase-1 , IL-1b , and IL-18 .
Conclusions: Results indicate that the expression of the NEK7-NLRP3 complex might play a protective role in the pathogenesis of SLE and is inversely correlated with disease activity. A positive effect of NEK7 on NLRP3 was observed, and the low expression of NLRP3 in SLE patients might be related to the low expression of NEK7 . Overexpression of Caspase-1 in SLE patients mediates the maturation and release of IL-1b and IL-18 , and contributes to the pathogenesis of SLE and LN.
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