Сytokine在SARS-CoV-2严重感染病例中的表达和产生

Natalya D. Abramova, E. A. Meremyanina, N. O. Kalyuzhnaya, A. V. Poddubikov, M. P. Kostinov, V. V. Grechenko, O. A. Svitich
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引用次数: 0

摘要

大多数呼吸道病毒感染以轻度形式进行,包括COVID-19。然而,一些患者会出现严重的全身性炎症、组织损伤、急性呼吸窘迫综合征和细胞因子风暴,这些都可能导致致命的后果。细胞因子被认为在病毒感染的免疫病理中起重要作用。然而,过度的免疫反应,表现为大量释放促炎细胞因子,可能导致机体免疫损伤。在健康个体中,细胞因子的产生和释放需要炎症和体内平衡因素的显著平衡。与此同时,在COVID-19疾病的情况下,细胞因子的产生不受控制地增加往往会给患者带来致命后果。这项工作的目的是研究IL-1、IL-18和TNF基因表达水平,以及这些细胞因子在上呼吸道粘膜水平的产生,特别是在口腔中,重症COVID-19患者。 本研究包括从严重COVID-19中康复的患者。对照组由条件健康个体组成。RT-PCR检测IL-1、IL-18、TNF基因表达水平。采用多重酶免疫分析法检测IL-1、IL-18和TNF蛋白生成水平。 IL-1、IL-18的表达水平在发病时和COVID-19病中期均有所降低,但在第30天升高。这些细胞因子的蛋白质产生在发病的头几天也减少了。在疾病发病时,促炎TNF细胞因子的水平很高。与对照组相比,发病时肿瘤坏死因子的产生水平也较高。随后,TNF基因表达水平随着疾病的进展而下降。 因此,促炎细胞因子的表达水平升高可能是由于SARS-CoV-2病毒的S蛋白诱导这些细胞因子在人单核细胞中的表达增加。与此同时,适当的蛋白质水平仍然很低,特别是在发病的第一天。因此,可以得出结论,病毒在发病后15-30天内引发热腐病,此时病毒复制已经很少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Сytokine expression and production in severe cases of SARS-CoV-2 infection
Most respiratory viral infections proceed in mild form including COVID-19. Gowever, some patients experience severe systemic inflammation, tissue damage, acute respiratory distress syndrome, and cytokine storm with potentially lethal outcomes. The cytokines have been thought to play an important role in immunopathology of viral infection. However, an excessive immune response, manifesting as massive release of pro-inflammatory cytokines, may cause immune damage in the body. Production and release of the cytokines in healthy individuals presumes a significant balance of inflammatory and homeostatic factors. Meanwhile, in the case of COVID-19 disease, uncontrolled increased production of cytokines often occurs with fatal consequences for patients. The aim of this work was to study the level of IL-1, IL-18 and TNF gene expression, as well as production of these cytokines at the level of mucous membranes of the upper respiratory tract, in particular in oral cavity, in patients with severe COVID-19 disease. The present study included patients who recovered from severe COVID-19. The control group consisted of conditionally healthy individuals. Expression levels of the IL-1, IL-18, and TNF genes were determined by RT-PCR. The levels of IL-1, IL-18 and TNF protein production were determined by multiplex enzyme immunoassay. The expression levels of IL-1, IL-18 were reduced at the onset of the disease, as well as in the midpoint of the COVID-19 disease, but increased on the 30th day. The protein production of these cytokines was also reduced in the first days from the onset of the disease. The levels of pro-inflammatory TNF cytokine was high at the onset of the disease. The level of TNF production at the onset of the disease was also higher relative to the control group. Subsequently, the TNF gene expression levels decreased upon progression of the disease. Thus, the increased expression level of pro-inflammatory cytokines may be explained by the fact that the S protein of the SARS-CoV-2 virus induces increased expression of these cytokines in human monocytes. Meanwhile, appropriate protein levels remain low, especially on day 1 from the onset of the disease. Thus, one may conclude that the virus triggers pyropotosis, however, within 15-30 days from the onset of the disease, when viral replication is already minimal.
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