In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli.
The release of histamine and leukotrienes can lead directly to bronchospasm. Episodic bronchospasm is associated with coughing, wheezing, tightness of the chest, and difficulty breathing. Symptoms decrease over time, sometimes lasting only a few minutes, but occasionally up to several days. In addition, the release of cytokines by mast cells, T-cells, fibroblasts, endothelial and epithelial cells, in turn, activates neutrophils, eosinophils and macrophages, which produce the chronic allergic inflammation characteristic of asthma Holgate (1999:27). Cytokines can also modulate smooth muscle responsiveness, modulate vascular permeability, activate neurons and stimulate mucus secretion. These effects can lead to the structural changes in the lung, i.e., vasodilatation; microvascular leakage; epithelial disruption; hypertrophy and hyperplasia of smooth muscle; and thickening of the airway wall as a result of new vessel formation, increased numbers of epithelial goblet cells, and deposition of interstitial collagen beneath the epithelium.
Asthma attacks are characterized by a bronchoconstrictor response to a wide variety of stimuli; among these stimuli is exposure to allergens which provoke an immunoglobulin E (IgE) dependent release of mediators from mast cells Holgate (1999:28). This bronchoconstrictor response along with mucus secretion and vascular leakage leads to the common clinical symptoms of wheezing, chest tightness and dyspnoea.
