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THU0257 Enhanced activation of NLRP3 inflammasomes in patients with SJÖGREN's syndrome
  1. JN Kim,
  2. S-K Kim,
  3. J-Y Choe
  1. Division of Rheumatology, Department of Internal Medicine, Catholic University of Daegu School of Medicine, Daegu, Korea, Republic Of

Abstract

Background There has been data about pathogenic role of NLRP3 inflammasome in Sjögren's syndrome. However, linkage between their clinical features and NLRP3 inflammasome has not been clearly defined.

Objectives The aim of this study is to identify the association of NLRP3 inflammasome with clinical features in patients with primary Sjögren's syndrome.

Methods A total 25 female patients with Sjögren's syndrome and gender-matched 25 healthy controls were consecutively enrolled. The mRNA expression for target genes including NLRP3, ASC, caspase-1, IL-1b, and IL-18 in peripheral blood mononuclear cells (PBMCs) were measured using real-time polymerase chain reaction. Serum IL-1b and IL-18 expression were also measured by ELISA method. Clinical information and disease activity and damage for Sjogren's syndrome such as EULAR Sjögren's Syndrome Disease Activity Index (ESSDAI) and Sjögren's Syndrome Disease Damage Index (SSDDI) were collected at the time of enrollment. Statistical analysis were applied including Spearman's correlation coefficient and Mann-Whitney t-test.

Results Patients with Sjögren's syndrome was found to be highly expressed in mRNA IL-1b and its protein, compared to controls (p<0.001 and p=0.001, respectively). The mRNA levels of caspase-1 and ASC were significantly higher than those in controls (p=0.021 and p=0.008, respectively), but not mRNA level of NLRP3. The mRNA level of IL-1b is closely related with mRNA level of NLRP3 and ESR (r =0.549, p<0.001 and r =0.577, p=0.003, respectively). Serum IL-1b protein expression in Sjögren's syndrome was found to be associated with mRNA level of caspase-1. Based on SSDDI, patients with SSDDI ≥1 was older and higher IL-1b and NLRP3 mRNA expression, compared to those with SSDDI =0 (p=0.035, p=0.005, and p=0.016, respectively).

Conclusions This study confirmed that activation of NLRP3 inflammasome might implicated the pathogenesis of Sjögren's syndrome.

Disclosure of Interest None declared

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