Abstract

Asthma is a chronic inflammatory disease of the lung of atopic individuals with an acute intermittent reversible obstructive airway disease [1]. This leads to wheeziness, chest tightness, obstruction of the lumen of the lower respiratory tract, bronchospasm, edema, thick secretions, accumulation of inflammatory cells [including mast cells and eosinophils] and hyperplasiahypertrophy of the smooth muscle and mucus secretion, exacerbating respiratory difficulties [1]. There are two major asthma types, allergic and non-allergic, with similar manifestations of inflammation and airway hyper-responsiveness, mediated by different mechanisms. By definition, allergic asthma is associated with allergensesitization, IgE-mediated hypersensitivity and Type2 immune responses (Th2-cells); while non-allergic asthma is associated with a neutrophilic inflammatory response and a Type1 (Th1-cells) and Type-17 (Th17-cells) cytokine profile. About 70% of cases of asthma involve mast cell reactions, mainly due to IgEmediated immediate hypersensitivity [2]. The number of cases and severity of asthma have been increasing without any plausible explanation. A large number of reports indicated that the pathophysiology of asthma is initiated by mast cell activation in response to allergen binding IgE receptor and TH2-cells [3]. This leads to cytokine generation by the mast cells and recruitment of eosinophils and

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