Role of Neutrophils in Idiopathic Pulmonary Fibrosis: A Literature Review

Abstract:

Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive lung disease characterised by continuous scarring of the lung parenchyma, resulting in reduced pulmonary function and impaired gas exchange. The pathophysiology of IPF reflects a combination of environmental factors, genetic predisposition, and ageing, which together contribute to repetitive alveolar epithelial cell injury and aberrant repair mechanisms. Neutrophils play a pivotal role in the progression of IPF by participating in both early inflammatory responses and late fibrotic processes. They release proinflammatory cytokines and proteolytic enzymes, including neutrophil elastase, and generate neutrophil extracellular traps (NETs), all of which exacerbate tissue injury and promote fibrogenesis. Clinical studies have demonstrated a correlation between elevated neutrophil counts and disease progression, underscoring their potential as biomarkers and therapeutic targets. A deeper understanding of the multifaceted role of neutrophils in IPF pathogenesis may facilitate the development of novel therapeutic strategies aimed at reducing inflammation and fibrosis, ultimately improving patient outcomes.