In addition, it has been demonstrated that alveolar macrophages with shortened telomeres from COPD patients exhibit mitochondrial damage, which induces oxidative stress; hyperactivation of the inflammasome; and elevated levels of proinflammatory cytokines such as IL-1β, TNF, IL-6, IL-8, monocyte chemotactic protein (MCP)-1, Hu-GRO, and intercellular adhesion molecule (sICAM)-1, which together perpetuate pulmonary inflammation during COPD [95,129,130]. Here, CCL2 is linked to chronic obstructive pulmonary disease.