Unknotting the crosstalk between COPD and neuroinflammation

COPD is a progressive respiratory illness that is mostly caused by air pollution, biomass fuel exposure, or long-term cigarette smoking. It is increasingly being referred to as a multisystem inflammatory disease rather than a pulmonary-only one. As a result of chronic airway inflammation in COPD, pro-inflammatory cytokines such as IL-1β, IL-6 and TNF-α are released throughout the body, causing systemic oxidative stress. Cardiovascular disease, skeletal muscular atrophy, osteoporosis, metabolic syndrome, and neurological impairment manifested as depression, anxiety, and cognitive impairment are among the several comorbidities associated with this systemic inflammation. Similarly, neuroinflammation, which is characterized by the activation of astrocytes and microglia that produce cytokines and ROS, causing neuronal damage and altered brain function, is closely linked to COPD, according to limitations. The integrity of the blood-brain barrier is also negatively impacted by chronic hypoxemia and due to oxidative stress in COPD, which permits inflammatory chemicals to enter the central nervous system and cause neurodegeneration. The systemic neural inflammatory connection is evident in the higher levels of biomarkers such as CRP, IL-6, and TNF-α in COPD. Thus, understanding the lung-brain axis provides valuable insight into the broader impact of COPD, and therapeutic approaches that reduce inflammation and oxidative stress may improve neurological and respiratory outcomes, offering a more all-encompassing approach to COPD management.