Role of inflammatory cells in airway remodeling in COPD

Abstract

COPD is characterized by chronic bronchitis, chronic airway obstruction, and emphysema, leading to a progressive and irreversible decline in lung function. Inflammation is central for the development of COPD. Chronic inflammation in COPD mainly involves the infiltration of neutrophils, macrophages, lymphocytes, and other inflammatory cells into the small airways. The contribution of resident airway structural cells to the inflammatory process is also important in COPD. Airway remodeling consists of detrimental changes in structural tissues and cells including airway wall thickening, epithelial metaplasia, goblet cell hypertrophy, and smooth muscle hyperplasia. Persistent airway inflammation might contribute to airway remodeling and small airway obstruction. However, the underlying mechanisms remain unclear. In this review, we will provide an overview of recent insights into the role of major immunoinflammatory cells in COPD airway remodeling.

Keywords: COPD; airway inflammation; airway remodeling.

Figure 1

Role of inflammatory cells in airway remodeling in COPD. Notes: Exogenous oxidants cause infiltration of inflammatory cells including neutrophils, macrophages, mast cells, and lymphocytes into the airway and lung tissue, resulting in excessive expression of some proteases and inflammatory mediators. This induces the accumulation of inflammatory cells into the airway, leading to the remodeling of airway structure. Abbreviations: ILC, innate lymphoid cell; MCP, monocyte chemoattractant protein; MMPs, matrix metalloproteinases; MPO, myeloperoxidase; NE, neutrophil elastase; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α; VEGF, vascular endothelial growth factor.