Inflammatory events in severe acute asthma

Abstract

Severe acute asthma can be induced by different triggers, allergens, irritants, viruses, etc., which induce inflammation and provoke acute bronchoconstriction. Inflammatory cells, such as activated eosinophils and neutrophils identified in sputum and bronchial lavages (BL) in severe acute asthma from children and adults are associated with increased levels of IL-5, IL-8, and of proinflammatory mediators. Viruses, but also endotoxin or allergen exposure, are able to recruit neutrophils, via an IL-8 production by activated macrophages or epithelial cells. Together, these inflammatory mediators are responsible for the diffuse bronchial inflammation, which involve large and small airways. Activated T cells may also be related to the pathogenesis of severe asthma. An aberrant CD8+ T lymphocyte response in bronchi, with a cytotoxic activity has been associated with fatal asthma. Moreover, the persistence of inflammatory cells in bronchi, particularly neutrophils, which respond poorly to corticosteroids, could be in part responsible for the epithelial damage, the extensive mucus plugging, and the abnormalities of epithelial and endothelial permeability which are associated with severe acute asthma. Further studies are necessary to better identify the implication of this increased bronchial permeability in the persistence of high levels of airway resistance, particularly in patients with status asthmaticus.