Clinica chimica acta; international journal of clinical chemistry · 2018
NLRP3 inflammasomes and NLRP3 inflammasome-derived proinflammatory cytokines in peripheral blood mononuclear cells of patients with ankylosing spondylitis.
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Kim Seong-Kyu, Cho Yoon Jeong, Choe Jung-Yoon
Аннотация
OBJECTIVE: There is some evidence that an enhanced Th17 response is attributable to interleukin-1β (IL-1β) matured by activation of the NLRP3 inflammasome. In this study, we assessed the expression of NLRP3 inflammasome components and their associated proinflammatory cytokines in patients with ankylosing spondylitis (AS).
METHODS: A total of 23 male patients with AS and 29 male controls were recruited and peripheral blood mononuclear cells (PBMCs) were collected. Transcript and protein expression of NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay, respectively. Data were analyzed using Spearman's correlation coefficient, Mann-Whitney U test, and receiver operating characteristic curves.
RESULTS: Higher mRNA expression of NLRP3, ASC, IL-1β, IL-17A, and IL-23 was noted in the PBMCs of AS patients than those of controls (p = 0.013, p = 0.001, p = 0.002, p = 0.011, and p = 0.037, respectively). Similarly, protein expression of NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 was higher in the AS group than the control group. There were significant correlations among NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 expression in patients with AS, except for a weak association between NLRP3 and IL-17A. Treatment of cultured PBMCs with 10 ng of lipopolysaccharide induced NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 expression, which was marked suppressed by treatment with ascorbic acid.
CONCLUSION: This study suggests that the NLRP3 inflammasome may be involved in the pathogenesis of AS and therefore a potential therapeutic target in AS.
METHODS: A total of 23 male patients with AS and 29 male controls were recruited and peripheral blood mononuclear cells (PBMCs) were collected. Transcript and protein expression of NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay, respectively. Data were analyzed using Spearman's correlation coefficient, Mann-Whitney U test, and receiver operating characteristic curves.
RESULTS: Higher mRNA expression of NLRP3, ASC, IL-1β, IL-17A, and IL-23 was noted in the PBMCs of AS patients than those of controls (p = 0.013, p = 0.001, p = 0.002, p = 0.011, and p = 0.037, respectively). Similarly, protein expression of NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 was higher in the AS group than the control group. There were significant correlations among NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 expression in patients with AS, except for a weak association between NLRP3 and IL-17A. Treatment of cultured PBMCs with 10 ng of lipopolysaccharide induced NLRP3, caspase-1, ASC, IL-1β, IL-17A, and IL-23 expression, which was marked suppressed by treatment with ascorbic acid.
CONCLUSION: This study suggests that the NLRP3 inflammasome may be involved in the pathogenesis of AS and therefore a potential therapeutic target in AS.