Farkhod Musaev
The immune reactivity of the body plays a significant role in the pathogenesis of airway inflammation in chronic obstructive pulmonary disease (COPD). Immunological changes are primarily associated with increased neutrophils, macrophages, and CD8+ T-lymphocytes. Key inflammatory mediators involved in COPD include interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a), and interleukin-8 (IL-8). Cytokines are protein mediators secreted by various immune cells in response to pathogens such as viruses, bacteria, and toxins, influencing the immune and inflammatory responses. This imbalance is a predictor of disease progression and severity. Furthermore, research has linked elevated levels of IL-1 fl, IL-6, and TNF-a in COPD patients to pulmonary hypertension, correlating with the severity of the disease and an increased risk of mortality. This review highlights the critical role of cytokines in the inflammatory and immune mechanisms underlying COPD pathogenesis. Understanding these molecular pathways may contribute to developing targeted therapeutic strategies to modulate cytokine activity to improve disease outcomes.
