Background information respiration | Pathophysiology | Morphology

Morphological changes leading to airflow limitation and airway obstruction

Morphological changes in asthma occur throughout the airway wall and the whole length of the bronchial tree. These changes affect airway epithelium, smooth muscles, matrix components, mucous glands, vessels and nerves.

Epithelial cells of asthmatics appear to be more fragile explaining the increased number of cells found in bronchoalveolar lavage. In general it is assumed that the epithelial-mesenchymal trophic unit is abnormally activated. Here upregulation of epidermal growth factor expression induced by mechanical stress present in active asthma seems to play a key role.

Reticular basement membrane thickening and deposition of matrix components below is a consistent finding in asthma. This kind of morphological change can occur before disease manifestation indicating that it is an early component in the pathological process. No association could be found between basement membrane thickening and age, symptom duration, forced expiratory volume or inhaled corticosteroid treatment. In all asthmatics the expression of transforming growth factor-b as well as the amount of collagen I and II are increased in the lamina propria while higher levels of interleukin 11 and 17 are only observed in moderate to severe asthma.

Proliferation of airway smooth muscles is predominantly caused by cell hypertrophy expressed in a nearly two-fold increase of smooth muscle cells in asthmatics. Smooth muscle proliferation may also drive airway fibrosis directly by transition of myocytes to fibromyocytes or indirectly by cytokine generation.

Goblet cell and submucosal gland cell hyperplasia are consistently found in the airways of asthmatics. Increased mucous secretion and an exsudate of serum proteins and cell debris combine to produce thickened plugs that may occlude the more peripheral airways. This phenomenon is most likely an important cause of airflow obstruction not responding to bronchodilator treatment.

In all forms of asthma mast cells and eosinophils appear to be the key effector cells of the inflammatory response. They have the capacity to secrete a wide range of preformed and newly generated mediators that act on airways directly or indirectly through neural mechanisms.

Airflow limitation in asthma also results from oedematous swelling of the airway wall. An increase of microvascular permeability and leakage results in mucosal thickening outside the smooth muscle layer. This again causes loss of elastic recoil pressure contributing to airway hyperresponsiveness.


O'Byrne P. GINA Executive Committee. Global strategy for asthma management and prevention. 2004. National Institutes of Health. Publication No 02-3659

Ward C, Pais M, Bish R, et al. Airway inflammation, basement membrane thickening and bronchial hyperresponsiveness in asthma. 2002. Thorax; 57: 309-316

Ward C, Walters H. Airway wall remodelling: the influence of corticosteroids. 2005. Curr Opin Allergy Clin Immunol; 5 (1): 43-48

Pathohistological changes in bronchial walls


Clicking on the expressions below highlights the corresponding structure
Smooth muscle cells
Hyaline cartilage
Connective tissue
Goblet cell
Mucus gland
Basal menbrane
Ciliated columnar epithel
Eosinophile granulocyte


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