Induction of Proinflamatuar Response by Pseudomonas aeruginosa Lipopolyssaccharide in Human Bronchial Epithelial Cells: Insights into Airway Inflammation

INTRODUCTION: Pseudomonas aeruginosa (P. aeruginosa) is a major opportunistic pathogen associated with chronic respiratory infections, particularly in individuals with compromised lung function such as those with 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.
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-α, and IFN-γ 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-α, and IFN-γ secretion were observed at 48 hours post-stimulation (p < 0.05), indicating a delayed but robust inflammatory response.
DISCUSSION AND 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.

Keywords: Pseudomonas aeruginosa, BEAS-2B, lipopolysaccharide, IL-6, TNF-α,, IFN-γ, airway inflammation, epithelial cells