Airway mucosa, submucosa and vessels in bronchial hyperresponsiveness

Schematic representation of elements of airway wall

As is the case with cartilage and smooth muscles, the mucosa, the submucosa and adventitia occupy space within the airway wall. The thickness of the airway wall internal to the airway smooth muscle will affect the degree of narrowing of the airway lumen. For the same degree of airway smooth muscle shortening, a thicker wall internal to the airway smooth muscle will result in greater luminal narrowing and a greater increase in airway resistance.

In asthma and COPD the smooth muscle layer and bronchial glands increase in size due to hypertrophy and hyperplasia. Chronic inflammation can further diminish airway patency by:

• Infiltration with inflammatory cells (leucocytes of various types, e.g. granulocytes, and lymphocytes).
• Inflammatory edema, i.e. an increase in interstitial water (Starling-Landis mechanism). This is due to vasodilation and associated higher hydrostatic pressures, increased vascular permeability, and the release of osmotically active substances.
• Thickening of the sub-basement membrane reticular layer underneath the epithelium.
• Hypertrophy and hyperplasia of glandular structures in the mucosa, often with increased production of sticky sputum which is not easily removed. This is often associated with intraluminal exudate. Removal may be compounded by epithelial damage (e.g. epithelial shedding in asthma), rendering mucociliary clearance less effective.
• Reduction in the forces of mechanical interdependence between the airways and lung parenchyma (through alveolar attachments) by swelling of the adventitia layer external to the airway smooth muscles.

For the same outer airway diameter, the inner diameter in a healthy subject will be larger than in subjects with asthma or COPD on account of the greater cell mass and interstitial water in the latter. When the smooth muscle contracts and the outer diameter diminishes, the incompressible components of the airway wall are displaced centripetally. For the same outer wall diameter and the same smooth muscle shortening, the inner airway diameter diminishes more dramatically the thicker the airway wall internal to the airway smooth muscle.

Note thick basal membrane under the epithelial layer, which is covered with much mucus in fatal case of status asthmaticus.
In this patient with fatal asthma the small airways show considerable hyperplasia and hypertrophy of smooth muscle, goblet cells and thickening of the mucosa. The airway wall is covered with unusually large amounts of mucus, and projects into the lumen like villi. With minimal additional smooth muscle shortening or edema the airway is fully closed.