Abstract
Background: Non-cystic fibrosis bronchiectasis (NCFB) is a chronic respiratory condition characterized by irreversible bronchial dilatation and persistent inflammation. Although inflammation plays a central role in disease progression, the upstream regulatory mechanisms remain incompletely understood. MicroRNA-155 (miR-155) is a well-recognized modulator of immune responses in chronic lung diseases, but its role in NCFB has not been previously elucidated. Methods: This study enrolled 58 NCFB patients and 30 healthy controls. The expression of miR-155 in peripheral blood mononuclear cells (PBMC) was quantified using qRT-PCR. Serum levels of IL-1β, IL-6, IL-8, and TNF-α were assessed by ELISA. Correlations between miR-155 expression and inflammatory cytokines, clinical indices, and Pseudomonas aeruginosa colonization were evaluated. In vitro, BEAS-2B epithelial cells were transfected with miR-155 mimics or inhibitors, and cytokine production was measured following LPS stimulation. Results: MiR-155 expression was significantly elevated in NCFB patients and positively correlated with IL-6, IL-8, TNF-α, and IL-1β levels (all p < 0.01). Higher miR-155 expression was also associated with increased disease burden, including elevated BSI scores and P. aeruginosa colonization. In vitro, miR-155 overexpression in BEAS-2B cells markedly enhanced pro-inflammatory cytokine secretion upon LPS stimulation, while inhibition of miR-155 suppressed cytokine release. Conclusion: miR-155 is upregulated in NCFB and closely associated with systemic and airway inflammation. It actively promotes pro-inflammatory signaling in airway epithelial cells, suggesting a pathogenic role in sustaining chronic inflammation. These findings highlight miR-155 as a potential biomarker of disease activity and a candidate target for immune modulation in bronchiectasis.