Airway Smooth Muscle in asthma pathogenesis Sample Clauses

Airway Smooth Muscle in asthma pathogenesis. Xxxxx and Xxxxxxx were the first to describe an increase in ASM tissue in the airways of asthmatics (Xxxxx & Xxxxxxxx 1922). Airway smooth muscle occupies a greater role in asthma patients than healthy individuals (Xxx et al. 2008) and is the most significant cellular change contributing to airway wall remodelling (Xxxxxxx et al. 1993). Increased smooth muscle mass in asthma may be caused by the proliferative and growth inducing effects of cytokines (Xxxxxxx & El Xxxxxx 2004). Multiple other mechanisms may contribute; including constitutional increases from birth caused by genetic, early life and environmental influences and decreased apoptosis/prolonged cell survival (Xxx & Xxxxxx 2005). Animal studies suggest that repeated chronic allergen exposure, causing airways inflammation can increase smooth muscle mass along with other features of airway remodelling (Xxxxx et al. 2004). On the other hand, once established, persistent AHR is likely to depend on the persistence of increased ASM mass which has the potential to dominate the mechanical response of the remodelled asthmatic airway (Xxxxxx et al. 2007), rather than the persistence of inflammation. It could therefore be argued that regulation of this remodelling is the most important therapeutic target especially for treatment of chronic, severe asthma. Xxxx et al assessed airway remodelling by determining the area and integrity of the epithelium, the smooth muscle mass, and the distance between the epithelium and ASM on bronchial biopsy tissues (Xxxx et al. 2005). It was found that ASM area was greater in subjects with severe asthma than in subjects with moderate asthma, and also the distance between the epithelial and ASM layers was less in the severe group than in the moderate group (Xxxx et al. 2005). They came to a conclusion that smooth muscle alteration is the key structural change that distinguishes severe asthma from moderate asthma. This altered structure might explain why patients with severe asthma are clinically more symptomatic when compared with subjects with moderate asthma (Xxxx et al.
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