Abstract
Background
Cell tight junction proteins create a barrier between airway epithelial cells to limit paracellular transport from the apical to basolateral surface. This barrier can impede the entry of respiratory pathogens and toxins from the airway lumen into the systemic circulation. Mast cell–mediated inflammation in the human airway can cause a disruption of this barrier. Tryptase is one of the major mediators released by mast cells and has been studied extensively in diseases such as asthma, reflux, and sinusitis. We hypothesize that tryptase may play a role in airway paracellular permeability by disrupting the cell tight junction proteins.
Methods
We tested this hypothesis by applying tryptase on the apical and basolateral surface to primary human airway epithelia grown in an air–liquid interface and measured changes in the transepithelial conductance and paracellular permeability of the membrane during short (every minute) and longer (over hours) time courses. We then immunostained the cell membranes for occludins and claudins to observe for changes in the structure of the tight junctions after tryptase application.
Results
Our data show that tryptase does not alter paracellular permeability in human airway cells over minutes or hours, and that tryptase does not alter the structure of the cell junction.
Conclusion
Tryptase alone does not alter paracellular permeability in human airway cells. Tryptase may be altering the epithelial membrane independent of the cell tight junction pathway or other mast cell mediators may play a role in permeability.
Keywords
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