Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Department of Medical Microbiology and Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Egypt J Immunol. 2022 Jul;29(3):90-98.
Severity of symptoms in COVID-19 has been shown to result from a cytokine storm. Interleukin (IL)-17 is one of these various cytokines, which results in a proinflammatory response, systemic inflammatory symptoms, inflammatory cell infiltration of lung tissue and thus leads to the massive lung pathology and multiorgan failure. Gene polymorphisms in the regulatory regions of cytokine-encoding genes affect the amounts of cytokines produced and possess a fundamental role in infectious diseases. This study aimed to investigate the role of IL-17A (rs2275913; G197A) gene polymorphism as predictor of disease severity and its correlation with IL-17 serum levels in COVID-19 patients. A group of 70 COVID-19 patients and 17 age and sex-matched control subjects were enrolled in the present work. Patients were classified into two groups moderate, severe and acute respiratory distress (ARDS) cases, defined according to the criteria established by the world health organization. Quantitative real time-polymerase chain reaction was done to detect IL-17A (rs2275913; G197A). Serum IL-17 levels were assessed by an enzyme-linked immunosorbent assay in both patients and controls. The distribution of different IL-17A G/A genotypes among COVID-19 patients were 44.3% for GG genotype, 44.3% for AG genotype and 11.4% for AA genotype. Genotypes among the control group were 43.8% for GG genotype, 50% for AG genotype and 6.3% for AA genotype. G allele distribution was 66.4%, 68.8% in patient and control group, respectively, and A allele was 33.6% and 31.3%, respectively. There was no association between the different genotypes, disease severity or IL-17 serum levels in the patient group. In conclusion, despite the possible role of IL-17 in the pathogenesis of inflammation, there was no association between IL-17 polymorphism and disease severity or IL-17 serum levels among Egyptian COVID-19 patients.
COVID-19 症状的严重程度已被证明是由细胞因子风暴引起的。白细胞介素（IL）-17 是这些细胞因子之一，它会导致促炎反应、全身炎症症状、肺部组织炎症细胞浸润，从而导致大量的肺部病理和多器官衰竭。细胞因子编码基因调节区的基因多态性影响细胞因子的产生量，并在传染病中起重要作用。本研究旨在探讨白细胞介素-17A（rs2275913；G197A）基因多态性作为 COVID-19 患者疾病严重程度预测因子及其与白细胞介素-17 血清水平的相关性。本研究纳入了 70 例 COVID-19 患者和 17 名年龄和性别匹配的对照者。根据世界卫生组织制定的标准，患者被分为中度、重度和急性呼吸窘迫（ARDS）病例两组。通过定量实时聚合酶链反应检测白细胞介素-17A（rs2275913；G197A）。通过酶联免疫吸附试验检测患者和对照组的血清白细胞介素-17 水平。COVID-19 患者中不同白细胞介素-17A G/A 基因型的分布为 GG 基因型 44.3%，AG 基因型 44.3%，AA 基因型 11.4%。对照组的基因型分别为 GG 基因型 43.8%，AG 基因型 50%，AA 基因型 6.3%。G 等位基因的分布分别为 66.4%和 68.8%，A 等位基因的分布分别为 33.6%和 31.3%。在患者组中，不同基因型、疾病严重程度或白细胞介素-17 血清水平之间无相关性。结论：尽管白细胞介素-17 可能在炎症发病机制中起作用，但在埃及 COVID-19 患者中，白细胞介素-17 多态性与疾病严重程度或白细胞介素-17 血清水平之间无相关性。
