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Titlebook: Cellular Mechanisms in Airways Inflammation; Clive P. Page,Katharine H. Banner,Domenico Spina Book 2000 Springer Basel AG 2000 asthma.brea

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Airway epithelial cells,role. Several studies have demonstrated that epithelial cells are capable of synthesising and releasing several biologically active mediators which directly or indirectly influence the activity of inflammatory cells important in allergic airway diseases, including allergic rhinitis and asthma [.].
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Drugs that reduce airways inflammation,teroids, disodium cromoglycate (DSCG), nedocromil sodium and theophylline have anti-inflammatory activity in asthmatics and also considers new drugs which are under development as potential anti-inflammatory agents for the treatment of bronchial asthma.
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Neutrophils,asis and a number of interstitial lung diseases. Thus, understanding the pro-inflammatory host defence functions of the neutrophil, and the mechanisms by which these are terminated, may yield insights into the pathogenesis of diseases which are a major cause of morbidity and mortality in the developed world.
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Pathological spectrum of airway inflammation,lung the air is sampled, conditioned, and rendered free of irritants and allergens before it reaches the respiratory portion of the lung. The cleansing function of the conducting airways depends upon its branching pattern and the dynamic interactions of structural cells, immuno-competent cells, and
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Eosinophils in asthma,g events in the airways, characterized by subepithelial deposition of collagen types III and V and fibronectin. This review discusses the mechanisms by which the cells are recruited to the airways and discusses the evidence for and against that eosinophilic inflammation is critical to the pathogenes
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T cells in the lung, phase response in the skin [.]. The airways of asthmatic patients are rich in T cells. In experimental animals, adoptive transfer of antigen-specific Th2 T cells and subsequent aerosol challenge are sufficient to induce inflammation and increase bronchial hyperresponsiveness [., .]. The cytokines p
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