Session Information
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Sjögren’s syndrome is a systemic autoimmune disease characterized by lymphocyte infiltration and subsequent dysfunction of exocrine glands, finally leading to dryness in the exocrine glands and dysfunction in the affected organs and tissues. The precise mechanism of Sjögren’s syndrome remains unclear. Recently, novel insight into the NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome that is responsible for innate immunity, has implicated it as a crucial regulator that plays a role in the pathogenesis of Sjögren’s syndrome. The aim of this study was to identify the association of NLRP3 inflammasome-induced inflammation with disease activity and damage in Sjögren’s syndrome.
Methods: A total of 33 female patients with Sjögren’s syndrome and 34 sex- and age-matched, healthy controls were consecutively enrolled. The mRNA expression levels of NLRP3, ASC, caspase-1, interleukin-1b (IL-1b), and IL-18 in peripheral blood mononuclear cells (PBMCs) were measured, as well as serum IL-1b and IL-18 protein expression levels. The EULAR Sjögren’s Syndrome Disease Activity Index (ESSDAI) and Sjögren’s Syndrome Disease Damage Index (SSDDI) were also evaluated.
Results: Patients with Sjögren’s syndrome group showed higher expression of mRNA IL-1b and IL-1b at the protein level than controls (p < 0.001 of both). The mRNA levels of caspase-1 and ASC were significantly increased in patients with Sjögren’s syndrome compared to controls (p = 0.001 and p = 0.002, respectively). Based on the SSDDI scores, patients with damage (SSDDI ≥ 1) had higher IL-1b mRNA expression compared to patients without damage (SSDDI = 0) (p = 0.034). SSDDI scores were closely related with IL-18 protein levels (r = 0.357, p = 0.041). The levels of IL-1b mRNA and IL-1b protein were correlated with the mRNA level of NLRP3 (r = 0.597, p < 0.001 and r = 0.502, p = 0.003, respectively). IL-1b mRNA expression was responsible for the presence of damage for Sjögren’s syndrome (p = 0.034).
Conclusion: This study confirmed that NLRP3 inflammasome-mediated inflammation might be implicated in the pathogenesis of Sjögren’s syndrome.
To cite this abstract in AMA style:
Kim SK, Choe JY, Park SH, Lee H. Enhanced Expression of NLRP3 Inflammasome-Related Inflammation in Peripheral Blood Mononuclear Cells in Sjögren’s Syndrome [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/enhanced-expression-of-nlrp3-inflammasome-related-inflammation-in-peripheral-blood-mononuclear-cells-in-sjogrens-syndrome/. Accessed .« Back to 2017 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/enhanced-expression-of-nlrp3-inflammasome-related-inflammation-in-peripheral-blood-mononuclear-cells-in-sjogrens-syndrome/