Enhanced expression of NLRP3 inflammasome-related inflammation in peripheral blood mononuclear cells in Sjogren's syndrome

Objective: The aim of this study was to identify the association of NLRP3 inflammasome-induced inflammation with disease activity and damage in Sjogren's syndrome. Methods: A total of 33 female patients with Sjogren's syndrome and 34 sex- and age-matched, healthy controls were consecutively enrolled. The mRNA expression levels of NLRP3, ASC, caspase-1, interleukin-1 beta (IL-1 beta), and IL-18 in peripheral blood mononuclear cells (PBMCs) were measured, as well as serum IL-1 beta and IL-18 protein expression levels. Protein levels for mature IL-1 beta (p17) and caspase-1 (p20) were analyzed by western blotting. The EULAR Sjogren's Syndrome Disease Activity Index (ESSDAI) and Sjogren's Syndrome Disease Damage Index (SSDDI) were also evaluated. Results: Patients with Sjogren's syndrome group showed higher expression of mRNA IL-1 beta and IL-1 beta at the protein level than controls (p < 0.001 of both). Enhanced expression of mature IL-1 beta (p17) and caspase-1 (p20) proteins in Sjogren's syndrome were noted, compared to controls. The mRNA levels of caspase-1 and ASC were significantly increased in patients with Sjogren'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-1 beta 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-1 beta mRNA and IL-1 beta protein were correlated with the mRNA level of NLRP3 (r = 0.597, p < 0.001 and r = 0.502, p = 0.003, respectively). IL-1 beta mRNA expression was responsible for the presence of damage for Sjogren's syndrome (p = 0.034). Conclusion: This study confirmed that NLRP3 inflammasome-mediated inflammation might be implicated in the pathogenesis of Sjogren's syndrome.