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.

Investigating the Effect of the Homeopathic Immunomodulator, MODUL8® on Blood Count, Bronchial Lavage and Fibrin Ultrastructure on Experimental Asthmatic BALB/c Mice

“…Increased eosinophil and T lymphocyte numbers in the broncho-alveolar lavage fluid are also characteristic of the inflammatory response in patients with asthma (Caramori et al, 2005;Tillie-Leblond et al, 2005;Walker et al, 1991). Up to 90% of the cells in the bronchial lavage of control mice are macrophages.…”

Pharmacotherapy of Asthma

“…4 Toward the end of the early phase of asthmatic response (3-8 hours), airway inflammation becomes more prominent. 5 Neutrophils, attracted by chemotaxis to the area of inflamed airway, leave the more permeable blood vessel and enter the respiratory tissues. Neurophils are joined by other inflammatory immune cells such as basophils, and eosinophils that escalate the inflammatory response by releasing their own inflammatory mediators.…”

A20 Attenuates Allergic Airway Inflammation in Mice

“…Nevertheless, there is still a subgroup of patients who have severe asthma that is resistant to corticosteroid therapy; this subtype of bronchial asthma is termed difficult-to-control or refractory asthma (3,4). These corticosteroid-resistant asthma patients are characterized by elevated levels of TNF-␣ (5, 6) and neutrophils (6,7), which can be treatment targets.…”