Effects of NF-κB Inhibition on Chronic Airway Epithelial Inflammation and Cell Migration

Background : Asthma is a chronic inflammatory airway disease characterized by mucus hypersecretion and structural remodeling, all of which contribute to airway obstruction. The NF-κB signaling pathway plays a central role in regulating inflammatory responses and epithelial dynamics. BAY11-7082, an NF- κB inhibitor, has been shown to modulate cytokine production, mucin expression, and epithelial cell migration. The objective of this study was to investigate the effects of NF-κB inhibition on the expression of inflammatory mediators, mucin production, and epithelial cell migration using human airway epithelial cell lines (Calu-3 and A549). Methods : Human airway epithelial cell lines A549 and Calu-3 were treated with BAY11-7082(as an NF-κB inhibitor), LPS (as an NF-kB activator), or both. Gene expression was assessed by qRT-PCR, mucus secretion by PAS staining, and cell migration by cell life imaging. Results : BAY11-7082 significantly reduced LPS-induced expression of pro-inflammatory cytokines (IL-6, IL-4) and mucins (MUC4, MUC5AC) in Calu-3 cells. BAY11-7082 significantly delayed cell migration compared to controls and LPS-treated groups, indicating strong suppression of epithelial cell movement ([ Fig. 1 ]). Cell viability assays confirmed that BAY11-7082 was non-toxic at tested concentrations. Conclusions : NF-kB inhibition by BAY11-7082 suppresses airway epithelial inflammatory responses, mucus hypersecretion, and cell migration in vitro. Targeting NF-kB signaling may represent a promising therapeutic approach, reducing both inflammation and aberrant epithelial remodeling. Fig. 1 Publication History Article published online: 04 March 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany