Bronchial mucosal permeability and its relationship to airways hyperreactivity.

The airways epithelium is made up of eight different cells with the ciliated cell, the microvillar or brush cell, and the goblet cells being the predominant cells forming the surface. These cells are joined by epithelial tight junctions and covered by a layer of mucus. The epithelium also contains an abundance of nerve fibres which are more concentrated in the extrathoracic airways. These irritant receptors or rapidly adapting stretch receptors run circumferentially around the surface cells and respond to a wide variety of stimuli including gases, smoke, dust, aerosols and antigens. While mast cells can be found in the airways lumen and in the epithelium, the greatest number are located in the submucosa. The epithelial surface barrier is normally quite impermeable to material that lands on it. However, a wide variety of injuries can induce inflammatory reactions and change the mucosal permeability to allow more easy access to the irritant receptors in the epithelia and mast cells in the submucosa. Injury by cigarette smoke induces an inflammatory reaction which causes an increase in mucosal permeability which returns to control values within a six-hour period. Maximal mucosal permeability is associated with the exudative phase of the inflammatory reaction where there is an increase in airways edema. By the time the polymorphonuclear leukocytes migrate to the mucosal surface, the permeability has returned to normal. These minimal inflammatory injuries are also associated with an increased cell turnover which may be responsible for the thickening of the basement membrane in chronic inflammatory states such as asthma.