الفهرس 
REVIEW OF LITERATUREOnly 14 pages are availabe for public view
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Abstract
Introduction: Bronchial Asthma is a T cell driven chronic inflammatory disorder of the airways. Both T helper-2 (Th2) and Th1 lymphocytes play an important role in the pathophysiology of asthma. Local overproduction of T helper Th2 cytokines (interleukin 4 (IL-4), IL-5, IL-9 and IL-13) by Th2 cells in the asthmatic airways is well defined and recent studies indicate that Th1 cells, secreting IFN γ, might cause severe airway inflammation Aim of work: Detection of the most common allergen in bronchial asthma patients. Detection of IL-17 in sputum of asthma patients and its correlation to disease severity and Corticosteroid therapy. Detection of apoptosis as an important item in allergic diseases and this will entails detection of serum Fas levels and effect of corticosteroid therapy on serum sFas level, and detection of sputum eosinophil apoptotic ratio (AR). Subjects and methods: The results of the present study showed higher levels of IL-17 in bronchial asthma patients [65.8(24-487) pg/ml] in comparison to healthy control [0 (0-7) pg/ml] with higher levels in severe asthma group [405(354.7-487.6) pg/ml] than mild [52.3 (24.8-90.2) pg/ml] and moderate asthma group [62.4 (45.5-88.3) pg/ml]. All healthy individuals had low to undetectable level of IL-17 in their sputum which make increased IL- 17 levels potentially useful as diagnostic aid in asthma, also there is positive correlation between the levels of IL-17 and the eosinophil percentage in the induced sputum from asthmatic patients which may suggest eosinophils as cellular source of IL -17. Results: These data suggest the role of IL-17 in bronchial asthma and its clinical implication in severe asthma and this led to hypothsis that targeting IL-17 may hold therapeutic potential in human asthma. The present study showed that serum concentration of sFas in asthmatic patients was significantly higher (1192.34 ± 795 pg/ml) than that of the healthy control subjects (367.64 ± 41.6 pg/ml) with statistically significant difference between the two groups (P < 0.001). Since sFas was shown to competitively inhibit the binding of membrane Fas antigen to Fas-ligand on the cell surface and, hence, to inhibit the Fas-mediated apoptotic pathway, the elevated serum concentrations of sFas in asthmatic patients might explain the down-regulated apoptosis of asthmatic T cells. The results of the present study showed that eosinophil AR is lower in bronchial asthma patients 0.61 ± 0.2 than control group (P <0.001) with inverse relationship between this AR and disease severity, eosinophil AR is decreased in severe asthma group than mild and moderate groups with statistically significant difference among these groups. Patients treated with inhaled corticosteroids showed increase in eosinophil AR. Also our results showed positive correlation between eosinophil AR and FEV1 as increased eosinophil apoptosis is associated with better pulmonary function tests. Conclusions: Induction of apoptosis by administration of anti –Fas antibody may have beneficial effect in removal inflammatory cells from airway.