ROLE OF NEUTROPHIL EXTRACELLULAR TRAPS IN ACUTE EXACERBATIONS OF COPD

Abstract

Acute exacerbations of chronic obstructive pulmonary disease (AECOPDs) represent pivotal events in the disease progression of COPD, significantly influencing patient morbidity and mortality. While traditionally attributed to infectious agents and environmental pollutants, emerging evidence highlights a central role of neutrophil extracellular traps (NETs) in exacerbation pathogenesis.For this reason, this study reviews and connects recent work on NETs’ correlation with AECOPDs.  When a neutrophil undergoes NETosis, it releases a network of DNA, histones and enzymes that surround pathogens and trigger events that damage lung tissue.  Markers of inflammation have been found to increase in the lungs and airways of COPD patients when they experience NETs.  In the study, it is noted that NETs like histones, neutrophil elastase and matrix metalloproteinases contribute to airway changes, break down the extracellular matrix and cause harm to both epithelial and endothelial cells.  Following NET’s formation, complement activation and inflammasome generation enable neutrophils to continue inflammation.  According to studies, NETs increase local inflammation after the first stimulus by producing more oxidative stress, drawing in more immune cells and increasing nearby cytokines.  NETs have a harmful effect in leading to small airway disease, fibrosis and emphysema which signal that COPD is becoming more severe.  This shows that NETs or their components might be useful in managing and preventing AECOPDs.  Moreover, this research finds that how neutrophils act in the lung may have a major role in COPD and that controlling NET formation may shape upcoming COPD treatments.