The airway epithelium CS events such as the first contact, long-term exposure to CS can induce epithelial cells to produce pro-inflammatory medium, senescence-associated secretory phenotype (MCP-1, IL-1, IL-6, IL-8), damage-associated molecular patterns (receptor for advanced glycation end-products, heat shock proteins, S100 proteins, high-mobility group box), the media which is released into the pulmonary and systemic circulation (9, 10), can stimulate the damage to the lung parenchyma, alveolar damage, and promote the development of COPD (11). Here, IL1B is linked to chronic obstructive pulmonary disease.