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Asthma pathophysiology

Although the mechanisms of asthma are complex and interactive, host factors (mainly genetic) primarily cause the development of asthma, while environmental factors usually trigger asthma symptoms (Figure 1).

11 fig 1Factors for the development of asthma
Figure 1: Host and environmental factors influence the development and expression of asthma

Asthma is an inflammatory disease, and it is this inflammation that is responsible for the symptoms associated with the disease. Activation of inflammatory cascades leads to hyperresponsiveness of the airways, with consequent airflow limitation and breathing difficulties. Inflammation also plays a key role in airway remodelling – a pathophysiological change observed with persistent inflammation.

11 fig 2Inflammatory cascade
Figure 2: The inflammatory cascade in asthma

The complex chain of molecular events which brings about inflammation in asthma involves many different cell types and mediators (Figure 2). The chronic inflammation causes irreversible changes in the airways, resulting in inelastic and narrow vessel walls (Figure 3) and significantly impairing lung function in affected patients.

In asthma, airways throughout the lung are affected by inflammation. These include the large bronchioles down to small airways (<2mm diameter); the latter make up a large proportion of total lung volume and contribute actively to asthma pathophysiology.1  

11 fig 3Airway remodeling
Figure 3: Chronic inflammation causes structural changes in both large and small airways1-3
Both images have been reproduced with permission from Elsevier.

References  
  1. Contoli M, Bousquet J, Fabbri LM, et al. The small airways and distal lung compartment in asthma and COPD: a time for reappraisal. Allergy 2010;65:141-51.
  2. Homer RJ, Elias JA. Airway remodeling in asthma: therapeutic implications of mechanisms. Physiology (Bethesda) 2005;20:28-35.
  3. Holgate ST, Polosa R. The mechanisms, diagnosis, and management of severe asthma in adults. The Lancet 2006;368:780-793. 
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