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Abstract Asthma is characterized as a chronic inflammatory disease of the bronchi, and it is well established that a variety of cells including mast cells, eosinophils, lymphocytes, basophils and epithelial cells play a role in this process.( Anthony et-al, 2000). However, there is a second way in which inflammatory cells can modify airway patency and responsiveness through the release of cytokines and chemokines. These molecules have profound and long lasting biologic effects in the microenvironment of their release and at distant sites. (Kathleen & Jeffrey, 1998). Segmental bronchoprovocation (SBP) with allergen provides a method to gain insight into the mechanism of allergic airway inflammation further more, the characteristics of the airway response to allergen can be helpful to identify differences between non asthmatic allergic diseases and bronchial asthma. (Nizar et al,1997). The EAR is considered to be largely mast cell dependant inducing the action of histamine, prostaglandin D2 and the sulphopeptide leukotrienes (LTC4, LTD4) and LTE4 whereas the LAR and the acquired , increase in BHR are considered to occurs secondary to the recruitment of inflammatory cells from the microcirculation. (Pierre et al; 1995). |