Abstract
COPD is associated with chronic inflammation of the airways, which causes damage to defense and repair mechanisms, resulting in remodeling processes in the bronchi and bronchioles. This leads to fibrosis of the lung tissue, increased smooth muscle tension, swelling of bronchial mucosa, loss of cilia function with accumulation of mucus, and finally to chronic pulmonary obstruction and possibly emphysema, with the main symptoms of dyspnea, coughing, and expectoration. Inhaled pollutants can activate immune cells like macrophages, T-lymphocytes, and subsequently neutrophilic granulocytes. Together, they release various pro-inflammatory messenger substances and enzymes. As a relevant example, they secrete proteases and disable antiproteases, an imbalance that destabilizes lung tissue. Of particular importance are several cytokines that are significantly elevated in the plasma of patients with COPD signals. In addition to the pathophysiologically clearly defined neutrophilic inflammation, there are also COPD patients with a predominantly eosinophilic inflammation, which could overlap with allergic bronchial asthma. Furthermore, inhaled pollutants can lead to oxidative stress, which increases inflammation and remodeling. Respiratory infections, in most cases bacterial infections, can trigger an exacerbation of already established COPD, in most cases bacterial infections. In addition to conventional medication, in case of refractory therapy, treatment with biologics could be an option.