{'fraction_non_alphanumeric': 0.040983606557377046, 'fraction_numerical': 0.03770491803278689, 'mean_word_length': 5.1033333333333335, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Activation Status of NLRP3 Inflammasome in Peripheral Blood Mononuclear Cells From Patients With Gout Flare.

BACKGROUND/OBJECTIVE
Although gout flares are featured by systemic signs of inflammation, cellular sources of inflammatory mediators are not yet properly characterized. Our objective was to evaluate serum levels and gene expression in peripheral blood mononuclear cells (PBMCs) of several molecules associated with the activation of NLRP3 inflammasome.


METHODS
Fifteen patients with gout flare and 15 individuals with asymptomatic hyperuricemia were cross-sectionally studied. Serum levels of interleukin 1β (IL-1β), IL-18, monocyte chemoattractant protein 1/chemokine (C-C motif) ligand 2 (CCL2), and vascular cell adhesion molecule 1 were measured as a reflection of systemic inflammation, whereas the expression of NLRP3, CASP1, IL18, and CCL2 genes was measured to assess the inflammatory characteristics of PBMCs.


RESULTS
Serum levels of IL-1β (1.27 [0.07-1.99] pg/mL vs. 0 [0-0.82] pg/mL, p = 0.032) and vascular cell adhesion molecule 1 (606 [435-748] pg/mL vs. 349 [305-422] pg/mL, p = 0.014) were significantly higher in patients with gout flare than in individuals with asymptomatic hyperuricemia, whereas differences in IL-18 and monocyte chemoattractant protein 1/CCL2 were not found. Notably, no differences were observed in the expression of NLRP3, CASP1, IL18, or CCL2 in PBMCs from individuals of one or another group.


CONCLUSIONS
Systemic inflammation during gout flares does not appear to be associated with NLRP3 inflammasome activation in PBMCs, suggesting that it may represent the systemic spread of local (synovial) inflammation to monosodium urate crystals, which provides a rationale for redirecting anti-inflammatory therapy from a systemic approach to one centered on the inflamed joint.