PD-1 and PDL-1 gene expression in nasal polyp tissue from patients with asthma exacerbated by non-steroidal anti-inflammatory drugs correlates with the severity of the disease

Abstract

<br><b>Introduction:</b> The clinical syndrome that includes asthma, nasal polyps and hypersensitivity to nonsteroidal anti-inflammatory drugs is referred to as airway disease exacerbated by nonsteroidal anti-inflammatory drugs. Patients usually have the most severe form of nasal polyps. Asthma and chronic rhinosinusitis with nasal polyps share a common inflammatory profile, involving type 2 helper T lymphocytes. T-cell activity can be inhibited via the programmed death receptor, PD-1, leading to modulation of the immune response. Therefore, the purpose of this study is to evaluate the expression of genes encoding PD-1 and its ligand PD-L1 in nasal polyp tissue in patients with asthma exacerbated by non-steroidal anti-inflammatory drugs and to correlate the results with clinical data. <br><b>Material and methods:</b> The material used for the study consisted of 54 tissue sections of nasal polyps. In the specimens, the expression of PD-1 and PD-L1 genes was determined at the mRNA level by qPCR. Statistical analysis was used to evaluate the results of the study.</br> <br><b>Results:</b> The expression of PD-1 and PD-L1 genes in the tissue of polyps was statistically significantly higher than in the nasal mucosa of patients in the control group. In addition, there was a correlation between the expression of both genes at the mRNA level and the severity of nasal polyps in the paranasal sinuses analyzed from computed tomography images of the paranasal sinuses and assessed using the Kennedy scale.</br> <br><b>Conclusions:</b> Determining the expression of PD-1 and PD-L1 genes may provide a marker for the severity of polypoid lesions. In addition, learning more about the PD-1/PD-L signaling pathway and how it can be modulated may provide a potential therapeutic strategy for patients with inflammatory diseases.</br>