Waterpipe smoke condensate activates autophagy in non-tumorigenic lung epithelial cells: implications for inflammation and stemness

We exposed non-tumorigenic human bronchial epithelial BEAS-2B cells to waterpipe smoke condensate (WPSC). WPSC reduced viability dose-dependently, but a subcytotoxic dose (0.1%) caused only a transient drop in viability and no significant apoptosis over 72 h (MTT and Annexin V/PI assays).

This resistance was associated with autophagy activation: LC3-II and p62 accumulated over time and further increased with bafilomycin A1, alongside increased AMPK and decreased mTORC1 phosphorylation. Blocking autophagy with bafilomycin A1 increased apoptosis and necrosis, indicating a protective role. WPSC also induced DNA damage (γH2AX and 53BP1 foci), proinflammatory cytokines (IL-1β, CCL2), and the cancer stem cell markers CD44 and CD133.