The role of eosinophilic leukocytes in pathogenesis of bronchial asthma

Abstract

Pathogenesis of bronchial asthma has not been completely understood. Eosinophilic leukocytes accumulate in high numbers in the lungs, blood and sputum of asthmatic patients. Peripheral blood eosinophilia has been identified as a risk factor for the development of airway obstruction. Prominent eosinophilic inflammatory infiltrate in the bronchial mucosa and correlation between eosinophil numbers and disease severity supports the hypothesis that eosinophils are central inflammatory cells capable of inducing pathophysiological features of asthma. Activated eosinophils secrete a wide range of preformed and newly generated mediators that damage the bronchial epithelium, contract smooth muscle, increase mucous secretion and cause vasodilatation. There is ample evidence that oxidants generation is increased during an asthma exacerbation. Many investigations indicate that airway and blood eosinophils produce more oxidants in asthmatic patients compared with control subjects.