The Role of

Background: Chronic obstructive pulmonary disease (COPD) is characterized by progressive airway inflammation and compromised immune defense, often worsened by reduced secretory immunoglobulin A (sIgA) levels. This decline in sIgA is linked to diminished polymeric immunoglobulin receptor (pIgR) activity, which impairs mucosal immunity. MicroRNA-144 (miR-144), a microRNA implicated in inflammation, may contribute to pIgR suppression, though this pathway in COPD remains poorly understood. Methods: Human bronchial epithelial cells were exposed to cigarette smoke extract (CSE) to mimic COPD conditions, and were subsequently divided into control and CSE-treated groups. miR-144 was either inhibited or overexpressed in these cells via transient transfection. Expression levels of miR-144, transforming growth factor beta-induced factor homeobox 1 (TGIF-1), transforming growth factor beta (TGF-β), and pIgR were analyzed using quantitative real-time polymerase chain reaction and Western blot. Additionally, a TGF-β inhibitor was applied to assess TGF-β's role in miR-144-mediated regulation of pIgR. Results: CSE treatment significantly upregulated miR-144 and TGIF-1 while reducing TGF-β and pIgR expression. miR-144 inhibition restored TGF-β and pIgR levels, while miR-144 overexpression reduced them further, indicating miR-144's direct influence on this regulatory pathway. TGF-β inhibition enhanced the reduction of pIgR under miR-144 overexpression, underscoring TGF-β's key role in pIgR regulation. Conclusion: miR-144 mediates immune suppression in COPD by downregulating pIgR through the TGF-β pathway, suggesting that miR-144 could serve as a therapeutic target to restore airway immune function and mitigate disease progression in COPD.