These inflammatory cells generate a range of mediators that act on target cells in the airways, and result in the abnormal pathophysiological features of Asthma (Barnes, 1996). The walls of the airways are considered to be oedematous, and are occupied by inflammatory cells (Barnes, 1996). The activated CD4 T-lymphocytes transport the leukocytes from the bloodstream to the airways (Holgate, 2008), and hence manage the release of mediators from lymphocytes, mast cells, and eosinophil (Fireman, 2003). The allergen trigger causes the cross linkage between the two IgE molecules, and hence results in the release of leukotriene, histamine, and other mediators. These mediators along with mast cells and eosinophil, which produce cytokines, propagate the inflammation of the airways (Fireman, 2003). Consequently, a bronchoscopy of an asthmatic airway is observed to be inflamed, indicating an increase in the number of mast cells, eosinophil, macrophage, and T-leukocytes. Evidence suggests a relationship between the degree of inflammation and the hyper-responsiveness (Barnes, 1996), which is recognised to be a decrease in bronchial airflow after broncoprovocation along with methacholine or histamine (Fireman,
These inflammatory cells generate a range of mediators that act on target cells in the airways, and result in the abnormal pathophysiological features of Asthma (Barnes, 1996). The walls of the airways are considered to be oedematous, and are occupied by inflammatory cells (Barnes, 1996). The activated CD4 T-lymphocytes transport the leukocytes from the bloodstream to the airways (Holgate, 2008), and hence manage the release of mediators from lymphocytes, mast cells, and eosinophil (Fireman, 2003). The allergen trigger causes the cross linkage between the two IgE molecules, and hence results in the release of leukotriene, histamine, and other mediators. These mediators along with mast cells and eosinophil, which produce cytokines, propagate the inflammation of the airways (Fireman, 2003). Consequently, a bronchoscopy of an asthmatic airway is observed to be inflamed, indicating an increase in the number of mast cells, eosinophil, macrophage, and T-leukocytes. Evidence suggests a relationship between the degree of inflammation and the hyper-responsiveness (Barnes, 1996), which is recognised to be a decrease in bronchial airflow after broncoprovocation along with methacholine or histamine (Fireman,