Abstract
Airway wall remodeling is a pathology occurring in chronic inflammatory lung diseases including asthma, chronic obstructive pulmonary disease, and fibrosis. In 2017, the American Thoracic Society released a research statement highlighting the gaps in knowledge and understanding of airway wall remodeling. The four major challenges addressed in this statement were: (i) the lack of consensus to define “airway wall remodeling” in different diseases, (ii) methodologic limitations and inappropriate models, (iii) the lack of anti-remodeling therapies, and (iv) the difficulty to define endpoints and outcomes in relevant studies. This review focuses on the importance of cell-cell interaction, especially the bronchial epithelium, in asthma-associated airway wall remodeling. The pathology of “airway wall remodeling” summarizes all structural changes of the airway wall without differentiating between different pheno- or endo-types of asthma. Indicators of airway wall remodeling have been reported in childhood asthma in the absence of any sign of inflammation; thus, the initiation event remains unknown. Recent studies have implied that the interaction between the epithelium with immune cells and sub-epithelial mesenchymal cells is modified in asthma by a yet unknown epigenetic mechanism during early childhood.
Highlights
Airway wall remodeling is a persistent pathology in asthma, which is resistance to treatment
This review focuses on the importance of cellcell interaction, especially the bronchial epithelium, in asthma-associated airway wall remodeling
It is unknown ing the lung to develop chronic inflammatory lung diseases later in life. It is unknown if theif the modification of specific genes leads to specific diseases, or if it is the nature of the second expomodification of specific genes leads to specific diseases, or if it is the nature of the second exposure to sure to risk factors that is decisive for the development of asthma or chronic obstructive pulmonary disease (COPD)
Summary
Airway wall remodeling is a persistent pathology in asthma, which is resistance to treatment. Tissue remodeling in the airways is the result of epithelial cell derangement, goblet cell hyperplasia, increased airway smooth muscle cells, thickening of the basal membrane, increased neovascularization in the sub-epithelial cell layers, and increased deposition of various extracellular matrix components [1]. It is currently unknown if specific structural changes characterize asthma pheno- and endo-types [2,3]. The cause of airway wall remodeling is not well understood, and most studies have investigated this pathology in adult asthma.
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