| Popis: |
Asthma is now one of the most common chronic diseases in westernised countries and is characterised by reversible airway obstruction, bronchial hyperresponsiveness and airway inflammation. Key pathological features include: infiltration of the airways by activated lymphocytes and eosinophils; damage to, and loss of, the bronchial epithelium; mast cell degranulation; mucous gland hyperplasia; and collagen deposition in the epithelial sub-basement membrane area. Asthma pathology is associated with the release of myriad pro-inflammatory substances including lipid mediators, inflammatory peptides, chemokines, cytokines, and growth factors. In addition to infiltrating leukocytes, structural cells in the airways, including smooth muscle cells, endothelial cells, fibroblasts and airway epithelial cells, are all important sources of asthma-causing or -enhancing mediators [1]. This complex scenario means that potential targets for therapeutic intervention are many and varied and the task of successful therapy a challenging one. |
