Background There has been data about pathogenic role of NLRP3 inflammasome in Sjögren9s 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 Sjögren9s syndrome. Methods A total 25 female patients with Sjögren9s 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 Sjogren9s syndrome such as EULAR Sjögren9s Syndrome Disease Activity Index (ESSDAI) and Sjögren9s Syndrome Disease Damage Index (SSDDI) were collected at the time of enrollment. Statistical analysis were applied including Spearman9s correlation coefficient and Mann-Whitney t-test. Results Patients with Sjögren9s 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 Sjögren9s 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 Sjögren9s syndrome. Disclosure of Interest None declared

OBJECTIVES:The aim of this study is to identify the prevalence of Behçet's disease (BD) from data in the Healthcare Bigdata Hub of the Health Insurance Review & Assessment (HIRA) Service from 2011 to 2015 in Korea.METHODS:This study collected information on primary and auxiliary diagnoses of BD (M352) by physicians according to the Korean Standard Classification of Diseases (KCD) codes. The prevalence of BD was assessed on the basis of age, sex, and geographical distribution. We used time series analysis, using the ARIMA model for the expected prevalence of BD from 2016 to 2025.RESULTS:The overall prevalence of BD was gradually increased, ranging from 32.8 to 35.7 per 100,000 population over the study period. The male to female ratio of BD ranged from 0.54:1 to 0.56:1, revealing a female predominance from 2011 to 2015. Among five districts in Korea, the prevalence in the Seoul Metropolitan district was the highest, with a slowly increasing trend for the study period, accounting for about 60.3% of total BD patients. The expected prevalence of BD patients was estimated to range from 36.9 (95% CI 35.0 - 39.0) to 44.7 (95% CI 40.2 - 49.6) between 2016 and 2025.CONCLUSIONS:This study found that the overall prevalence of BD is estimated to be approximately 35.0 per 100,000 population, with female predominance, and predicts gradually increased prevalence of BD in Korea.

Background Ellagic acid (EA) is a phenolic constituent in fruits and nuts, such as raspberries, strawberries, walnuts, mango kernel and pomegranate. It was documented that EA shows anti-fibrotic, anti-inflammatory activity in vivo model of bowel inflammation and lung fibrosis, however the precise mechanism of signal inhibition was not extensively investigated. Objectives The objectives of this study are first, to elucidate the anti-inflammatory effect of EA in RAW 264.7 murine macrophage cell line by NF-kB pathway in vitro, and second, to compare it with effect of other immuno-modulating agent, tacrolimus and colchicine. Methods We determined the cytotoxic effect of EA using MTT assay. The effects of EA on tumor necrosis facor (TNF)-alpha induced mRNA and protein expression were investigated using quantitative real-time PCR and western blot. In addition, we examined the effects of pharmaceutical drugs with anti-inflammatory properties on expression of TNF-alpha. Results EA significantly suppressed the expression of interleukin-1 beta and TNF-alpha in a dose dependent manner. EA suppressed TNF-alpha induced inflammatory genes expression by inhibiting the phosphorylation of JNK and Akt, whereas had no significant effect on p38 activation. In addition, the inhibitory effect of EA on TNF-alpha induced inflammatory genes expression was regulated by suppression of IkB-alpha phosphorylation and NF-kB translocation. The expression of TNF-alpha mRNA level was reduced comparably treated with EA and other anti-inflammatory agents (ascorbic acid, dexamethasone and colchicine). Conclusions These findings suggest that EA suppresses inflammatory genes expression through phosphorylation of JNK/Akt and regulation of NF-kB signal pathway in TNF-alpha induced inflammation. Further investigation regarding effects of EA on autoimmune, inflammatory is scheduled. References S. Corbett, J. Daniel, R. Drayton, M. Field, R. Steinhardt, N. Garrett, Evaluation of the anti-inflammatory effects of ellagic acid, J. Perianesth. Nurs. 25 (2010), 214–220. S. Ahmed, A. Rahman, M. Saleem, M. Athar, S. Sultana, Ellagic acid ameliorates nickel induced biochemical alterations: diminution of oxidative stress, Hum. Exp. Toxicol. 18 (1999) 691–698. Disclosure of Interest None declared