IL-17A )rs2275913; G197A) gene polymorphism as predictor for disease severity and its correlation with IL-17 serum levels in COVID-19 patients

Abstract

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.

Investigation of the relationship between IL17A, IL17F and ILR1N polymorphisms and COVID‐19 severity: The predictive role of IL17A rs2275913 polymorphism in the clinical course of COVID‐19

“…Rushdy et al. (2022) found no relationship between IL17A rs2275913 polymorphism and disease severity in their study of Egyptian patients with COVID‐19. Their patient group is comparatively smaller, and they divided patients into two groups according to disease severity.…”

“…Additionally, it has been shown that the IL-17 level relates to the ratio of partial pressure of arterial oxygen to the fraction of inspired oxygen (PaO2/FiO2) of patients with ARDS (Li et al, 2016). Rushdy et al (2022) found no relationship between IL17A rs2275913 polymorphism and disease severity in their study of Egyptian patients with COVID-19. Their patient group is comparatively smaller, and they divided patients into two groups according to disease severity.…”

“…In addition, Rushdy et al. (2022) determined that IL17F rs763780 polymorphism correlated with the prevalence of COVID‐19. The IL17A rs2275913 polymorphism is located between the binding sites of a transcription factor for the nuclear factor of activated T cells (NFATC), and it encourages the production of IL‐17.…”

MicroRNA-155 and 194 alter expression of Th17 and T regulatory-related transcription factors in the patients with severe coronavirus disease 2019 (COVID-19)

“…Prior studies have also shown the development of the Th17 subset in hospitalized SARS-CoV-2 infected patients ( Pourgholaminejad et al, 2022 , Sarmiento-Monroy et al, 2021 ). It is important to remember that some studies indicated that IL-17A is not up-regulated in hospitalized SARS-CoV-2 infected patients and that IL-17A did not significantly contribute to the induction of inflammation in some patients ( Rushdy et al, 2022 , Gupta et al, 2022 , Resende et al, 2022 , Maione et al, 2021 ). Our results also confirmed the results and revealed that IL-17A and its downstream molecules, IL-8 and CCL20, are down-regulated in the patients.…”

“…According to the findings, it appears that increased RORγt expression may be linked to faster cell growth, which may be a major factor in the induction of excessive inflammation in hospitalized SARS-CoV-2 infected patients. Previous studies showed that the hypercytokinemia storm in hospitalized SARS-CoV-2 infected patients significantly increased the amount of IL-17A, the primary cytokine produced by Th17 ( Shibabaw, 2020 , Ahmed Mostafa et al, 2022 , Rushdy et al, 2022 ). Prior studies have also shown the development of the Th17 subset in hospitalized SARS-CoV-2 infected patients ( Pourgholaminejad et al, 2022 , Sarmiento-Monroy et al, 2021 ).…”