Introduction: Poly (I:C) is a synthetic double-stranded RNA, a TLR3 ligand and mimic of viral infection. Epithelial cells exposed to poly (I:C) release inflammatory cytokines (e.g. IL-6) and display delayed wound healing. miR-149-5p may regulate inflammation and targets transcription factor p63, a key regulator of airway epithelium wound repair.

Aims: To determine the role of miR-149-5p in inflammatory responses and regulation of p63 in bronchial and alveolar epithelial cells exposed with poly (I:C).

Methods: Bronchial (BEAS-2B) or alveolar (A549) epithelial cell lines were maintained as submerged culture in BEBM supplemented with insulin-transferrin-sodium selenite, linoleic-BSA (ITS+1: 1%) or F-12K with ITS+1 (1%) during stimulation with poly (I:C, 0.5 µg/ml) for 48h, respectively. Cell viability was determined by lactate dehydrogenase release. miR-149-5p expression was assessed using TaqMan assay. IL-6 release and p63 expression were determined by ELISA and immunoblotting techniques, respectively.

Results: Poly (I:C) stimulation caused a significant BEAS-2B cell death after 24 and 48h stimulation but showed no effect on A549 cell viability. BEAS-2B cells exposed to poly (I:C) expressed lower level of miR-149-5p expression, which was correlated with increased IL-6 release and p63 expression and after 24 and 48h, respectively. Ectopic expression of miR-149-5p mimic in BEAS-2B cells, suppressed p63 after 48h. Although miR-149-5p expression was supressed in A549 cells stimulated with poly (I:C) after 48h, the IL-6 release and p63 expression remained undetected.

Conclusion: miR-149-5p may regulate IL-6 and p63 expressions. BEAS-2B cells respond differently to poly(I:C) compared with A549 cells.