Increased NLRP3 inflammasome expression in peripheral blood mononuclear cells of patients with schizophrenia: a case-control study

被引:4
作者
Unal, Gulin Ozdamar [1 ]
Ozturk, Kuyas Hekimler [2 ]
Inci, Huseyin Emre [1 ]
机构
[1] Suleyman Demirel Univ, Fac Med, Dept Psychiat, Isparta, Turkey
[2] Suleyman Demirel Univ, Fac Med, Dept Med Genet, Isparta, Turkey
关键词
Schizophrenia; NLRP3; P2X7R; inflammasome; IL-1; beta; IL-18; ANTIINFLAMMATORY AGENTS; SYMPTOMS; RECEPTOR; ASSOCIATION; INVOLVEMENT; ACTIVATION; DISORDERS; PATHWAY; RISK;
D O I
10.1080/13651501.2022.2106245
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objective: This study aimed to evaluate the gene expression of the P2X purinoceptor 7 (P2X7R)- nod-like receptor pyrin domain-containing protein 3 (NLRP3) signal pathway in peripheral blood mononuclear cells (PBMCs) between schizophrenia (SCZ) patients and healthy controls (HC) to reveal its relationship with clinical variables. Methods: Thirty-two SCZ patients and 41 healthy controls were included in this study. The Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of Negative Symptoms (SANS), The Global Assessment of Functioning (GAF) scale and the Functioning Assessment Short Test (FAST) scales were applied. P2X7R, NLRP3, IL-1 beta and IL-18 gene expression levels were evaluated by real-time polymerase chain reaction in PBMCs. Results: NLRP3, P2RX7, IL-1 beta and IL-18 expression levels were significantly higher in PBMCs of SCZ patients than in HC subjects. Negative correlations were found between NLRP3 gene expression levels and GAF and FAST scales scores. There was a negative correlation between IL-18 expression levels and the GAF and FAST scales scores and a positive correlation with the SAPS scale scores. Conclusions: Systemic inflammation is implicated in SCZ pathogenesis, according to our findings, which suggest that the NLRP3 pathway may be involved. The NLRP3 inflammasome may serve as a biomarker for SCZ, and its pharmacological regulation may be a promising treatment approach.
引用
收藏
页码:111 / 117
页数:7
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