Our findings further demonstrate the cellular senescence-associated inflammatory phenotype as one of the pathobiological mechanisms for the progression of COPD/emphysema, as the levels of pro-inflammatory cytokines (i.e., IL-6, IL-8, KC and MCP-1) were concurrently increased in CSE-treated human lung epithelial cells in vitro and elastase-exposed mouse lungs in vivo. Here, CCL2 is linked to pulmonary emphysema.