Inflammasomes are a group of molecules that are strongly involved in causing inflammation. This study aimed to evaluate the expression of NLR family pyrin domain containing 1 (NLRP1), NLRP3, and Apoptosis-associated speck-like protein containing a CARD (ASC) as well as their association with serum level of interleukin (IL)-1β in patients with coronavirus disease 2019 (COVID-19). Thirty COVID-19 patients and 30 healthy subjects (HS) were recruited. Peripheral blood specimens were collected from subjects to assess NLRP1, NLRP3, and ASC gene expression by Real time-PCR technique. Serum levels of IL-1β were also measured via the enzyme-linked immunosorbent assay (ELISA). The findings showed no significant differences in serum IL-1β level between COVID-19 patients and the HS group. mRNA expression of ASC (P = 0.008) and NLRP1 (P = 0.03) gene had a significant increase in COVID-19 patients compared to HS, while there was no significant increase in the expression of NLRP3 between the studied group. There were significant correlations between patient’s data and expression levels of NLRP1, NLRP3, IL-1β, and ACS. NLRP1 and ASC may have a more critical role in the generation of the active form of IL-1β in COVID-19 patients compared to NLRP3. However, serum levels of IL-1β in patients did not show a significant increase, which may be due to the patient’s condition and the application of virus escape mechanisms through impaired NLRP3 expression and its malfunction.

中文翻译：

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COVID-19患者血清白细胞介素1β水平与炎症小体相关基因表达的关系评估

炎症小体是一组与引起炎症密切相关的分子。本研究旨在评估 NLR 家族热蛋白结构域 1 (NLRP1)、NLRP3 和含有 CARD 的凋亡相关斑点样蛋白 (ASC) 的表达及其与血清白细胞介素 (IL)-1β 水平的关系。 2019 年冠状病毒病 (COVID-19) 患者。招募了 30 名 COVID-19 患者和 30 名健康受试者 (HS)。采集受试者的外周血标本，通过实时 PCR 技术评估 NLRP1、NLRP3 和 ASC 基因表达。还通过酶联免疫吸附测定 (ELISA) 测量了 IL-1β 的血清水平。研究结果显示，COVID-19 患者和 HS 组之间的血清 IL-1β 水平没有显着差异。与HS相比，COVID-19患者中ASC（P = 0.008）和NLRP1（P = 0.03）基因的mRNA表达量显着增加，而研究组之间NLRP3的表达量没有显着增加。患者数据与 NLRP1、NLRP3、IL-1β 和 ACS 表达水平之间存在显着相关性。与 NLRP3 相比，NLRP1 和 ASC 在 COVID-19 患者中活性 IL-1β 的生成中可能发挥更重要的作用。然而，患者血清中IL-1β水平并未出现显着升高，这可能是由于患者的病情以及通过NLRP3表达受损及其功能障碍而应用病毒逃逸机制所致。