The following is a summary of “Mast cell chymase regulates extracellular matrix remodeling-related events in primary human small airway epithelial cells,” published in the December 2022 issue of Allergy and Clinical Immunology by Zhao, et al.

Although mast cells are thought to be involved in the etiology of asthma, the exact processes were unclear. Mast cells may relocalize to the epithelial layer under asthmatic settings, which may have an impact on the functional characteristics of the airway epithelial cells. Chymase and tryptase are two of the several proteases that activated mast cells release from their secretory granules. For a study, researchers sought to determine the effects that these proteases could have on airway epithelial cells.

Tryptase or chymase was applied to primary small airway epithelial cells, and the effects on the cells’ survival, proliferation, migration, cytokine secretion, and transcriptome were assessed.

Tryptase was relatively resistant to the airway epithelial cells. In contrast, chymase significantly changed several aspects of the epithelial cells, with an emphasis on activities connected to the remodeling of the extracellular matrix (ECM). These included ECM-related genes like matrix metalloproteinases, whose reduced expression was validated at the protein level. Additionally, chymase inhibited the fibronectin gene’s expression and led to the breakdown of fibronectin produced by the epithelial cells. Additionally, it was shown that chymase inhibits the ability of airway epithelial cells to migrate and destroys the cell-cell contact protein E-cadherin on the surface of the epithelial cell.

The research suggested that chymase may have an influence on how airway epithelial cells regulate ECM remodeling processes, which might have repercussions for how mast cells affect inflammatory lung illnesses like asthma.