Cadmium-induced ER stress and inflammation are mediated through C/EBP–DDIT3 signaling in human bronchial epithelial cells

Insights into the molecular mechanisms behind smoking-induced cellular stress and inflammation may inform new therapies for lung disease. Cadmium (Cd) is a major component of cigarette smoke, and triggers chronic lung diseases by disrupting the normal function of airway cells. However, exactly how Cd affects cells is not well understood. Using cultured cells from the lining of the human bronchi, Seok-Ho Hong at Kangwon National University in Chuncheon, Korea, and co-workers identified genes that are altered after exposure to Cd. The genes affected were associated with cell division and duplication, cell death and oxidative stress mechanisms. Hong's team also identified a signaling pathway that mediates stress induced by Cd exposure. Suppressing a gene activated by this pathway alleviated Cd-induced stress and inflammatory responses, indicating the pathway could be a target for lung disease therapies.