Sampson, A. P. (2001) Eosinophils: Provokers or bystanders in asthma? Clinical and Experimental Allergy Reviews, 1 (2), 73-76. (doi:10.1046/j.1472-9725.2001.00010.x).
Abstract
Until the late 1970s, eosinophils were thought to have a beneficial role in the asthmatic airway by phagocytosing allergen debris and effete inflammatory cells. During the 1980s, evidence began to point to eosinophils as critical players in severe and persistent asthma, and studies in man and in animals since the 1990s have implicated Th-2-type cytokines as key inducers of airway eosinophilia and bronchial hyperresponsiveness (BHR).
The impact of eosinophilic inflammation on asthma pathophysiology has been increasingly questioned, particularly by studies that appear to disrupt the putative links between airway eosinophilia, bronchial hyperresponsiveness and airway remodelling. Both the extent and the pathophysiological importance of airway remodelling in asthma continue to be disputed, but recent studies suggest that remodelling is due to pathways distinct from those that cause eosinophil-mediated bronchoconstriction and epithelial damage.
In addition, there is increasing recognition that distinct patterns of leukocyte cellularity in the airway may underlie the diverse clinical phenotypes of asthma, with neutrophils and macrophages implicated as effector cells in subgroups of patients. This paper will assess the evidence for provoker and bystander roles of eosinophils in asthma, and focus particularly on eosinophils as the putative source of cysteinyl-leukotrienes (cys-LT) in a major subpopulation of asthmatics, who may represent the optimal target population for LTRA therapy.
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