Abstract

Introduction: Chronic obstructive pulmonary disease (COPD) is associated with persistent airway inflammation and an increased risk of adverse outcomes following coronavirus disease 2019 (COVID-19). While the lower airways have been the primary focus of most studies, the upper respiratory tract plays a critical role in SARS-CoV-2 entry and early symptom development. Inflammatory mediators, including interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and C-reactive protein (CRP), as well as the viral entry–related protease TMPRSS2, are involved in both COPD-associated inflammation and COVID-19 pathogenesis. This study investigated the expression of these markers in COVID-19 patients with underlying COPD. Materials and Methods: In this case–control study, peripheral blood samples were collected from COVID-19 patients with a documented history of COPD and from age- and sex-matched healthy controls. Total RNA was extracted, reverse transcribed into cDNA, and relative mRNA expression levels of IL-6, MCP-1, CRP, and TMPRSS2 were quantified using real-time polymerase chain reaction. Statistical analyses were performed using parametric tests, with statistical significance defined as p < 0.05. Results: Compared with healthy controls, COVID-19 patients with COPD demonstrated significantly higher mRNA expression levels of IL-6, MCP-1, and CRP (p < 0.05). TMPRSS2 expression was also elevated in the patient group, indicating a potential contribution to enhanced viral entry. Overall, the findings revealed a distinct inflammatory expression profile in patients with COPD during SARS-CoV-2 infection. Conclusion: The increased expression of IL-6, MCP-1, CRP, and TMPRSS2 in COVID-19 patients with underlying COPD suggests a combined effect of chronic inflammation and viral entry mechanisms. These markers may be valuable as accessible blood-based indicators of disease severity, although further studies are needed. Keywords: COVID-19; COPD; Gene expression; IL-6; MCP-1; TMPRSS2; C-reactive protein.

DOI: http://doi.org/10.18502/jcr.v13i2.22546