Aysegul YILMAZ, Utku YAKA
Van Medical Journal - 2026;33(1):8-13
Introduction: Pseudomonas aeruginosa is a prominent opportunistic pathogen frequently implicated in persistent respiratory infections, especially among patients with impaired pulmonary function, including those suffering from cystic fibrosis, bronchiectasis, or ventilator-associated pneumonia. The airway epithelium serves as a primary site for host-pathogen interaction and actively contributes to innate immune responses via the production of proinflammatory cytokines. This study aimed to evaluate the dose-dependent and temporal effects of P. aeruginosa lipopolysaccharide (LPS) on inflammatory gene expression and cytokine secretion in BEAS-2B bronchial epithelial cells. Materials and Methods: BEAS-2B cells were treated with increasing concentrations of P. aeruginosa LPS, and the optimal non-toxic dose was determined. Subsequently, cells were stimulated with 100 µg/mL LPS and harvested at 12, 24, 48, and 72 hours to assess the mRNA expression levels of IL-6, TNF-alpha, and IFN-gamma using qRT-PCR. Cytokine secretion into the culture medium was quantified by ELISA. Results: Stimulation with P. aeruginosa LPS significantly increased the expression and secretion of proinflammatory cytokines in a time-dependent manner. The highest levels of IL-6, TNF-alpha, and IFN-gamma secretion were observed at 48 hours' post-stimulation (p < 0.05), indicating a delayed but robust inflammatory response. Conclusion: These findings demonstrate that P. aeruginosa LPS elicits a marked proinflammatory response in human bronchial epithelial cells, highlighting the pivotal role of the epithelium in airway inflammation. The BEAS-2B cell line provides a valuable in vitro model for dissecting early immune responses to bacterial pathogens in the respiratory tract.
