当前位置: X-MOL 学术Immunobiology › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Inflammasome activation by NLRP1 and NLRC4 in patients with coronary stenosis.
Immunobiology ( IF 2.8 ) Pub Date : 2020-04-04 , DOI: 10.1016/j.imbio.2020.151940
Maria Eduarda de Albuquerque Borborema 1 , Sergio Crovella 1 , Dinaldo Oliveira 2 , Jaqueline de Azevêdo Silva 1
Affiliation  

Objective and design

We performed an experimental, analytical and prospective study to evaluate the systemic activation of inflammasome in atherosclerosis’ patients, in order to shed light into responsible mechanisms for plaque formation.

Subjects

We included sixty individuals distributed into 3 groups: 2 groups based on the report from the angiography (severe lesions - SL and primary lesions - PL) and 1 group enclosing healthy individuals (HC).

Methods

The expression assays of inflammasome genes NLRP1, NLRC4, CASP-1 and IL-1β were performed using Real Time qPCR, with specific Taqman Assays. IL-1β serum levels were analysed by commercial kit. Were applied the Shapiro-Wilk and Student’s T-test as statistical tests. Statistical significance was set to p ≤ 0.05.

Results

Upregulation of NLRP1 (+3.47 FC, p = 0.0001), NLRC4 (+7.06 FC, p = 6.792 × 10−09) and IL-1β (+2.43 FC, p = 0.005) was observed in all atherosclerosis patients when compared to HC. According to stenosis severity, patients with primary lesions showed upregulation of inflammasome genes NLRP1 (+2.87 FC, p = 0.0008), NLRC4 (+6.34 FC, p = 4.134 × 10-07) and IL-1β (+3.39 FC, p = 0.0012) with respect to the HC group. No statistical difference was found in IL-1β serum levels according the assessed groups.

Conclusions

Inflammasome activation in atherosclerosis’s patients can be systemic altered and may be triggered by NLRP1 and NLRC4 receptors. IL-1β gene expression was identified in our study as an important systemic detectable marker of plaque severity.



中文翻译:

NLRP1 和 NLRC4 在冠状动脉狭窄患者中激活炎症小体。

目标和设计

我们进行了一项实验性、分析性和前瞻性研究,以评估动脉粥样硬化患者炎症小体的全身激活,以揭示斑块形成的相关机制。

科目

我们将 60 个人分为 3 组:基于血管造影报告的 2 组(严重病变 - SL 和原发病变 - PL)和 1 组包含健康个体 (HC)。

方法

炎性体基因NLRP1NLRC4CASP-1IL-1β 的表达分析使用实时 qPCR 和特定的 Taqman 分析进行。通过商业试剂盒分析IL-1β血清水平。应用 Shapiro-Wilk 和 Student 的 T 检验作为统计检验。统计显着性设置为 p ≤ 0.05。

结果

与所有动脉粥样硬化患者相比,NLRP1 (+3.47 FC, p = 0.0001)、NLRC4 (+7.06 FC, p = 6.792 × 10 -09 ) 和IL-1β (+2.43 FC, p = 0.005)上调. 根据狭窄的严重程度,原发灶患者炎性体基因NLRP1 (+2.87 FC, p = 0.0008)、NLRC4 (+6.34 FC, p = 4.134 × 10 -07 ) 和IL-1β (+3.39 FC, p= 0.0012) 相对于 HC 组。根据评估组,IL-1β血清水平没有发现统计学差异。

结论

动脉粥样硬化患者的炎症小体激活可能会发生全身性改变,并且可能由 NLRP1 和 NLRC4 受体触发。在我们的研究中,IL-1β基因表达被确定为斑块严重程度的重要全身可检测标志物。

更新日期:2020-04-21
down
wechat
bug