The release of inflammatory mediators primes adhesion molecules on the airway epithelium and capillary endothelium, allowing inflammatory cells, such as eosinophils, neutrophils, and basophils, to adhere to the epithelium and endothelium, and subsequently migrate to the tissues of the respiratory tract. It is currently known that the airway epithelium is not only a passive barrier but an essential part of the local immune response in the airways, bridging innate and adaptive immunity against various environmental insults. In cases of sudden-onset, as is often with near fatal asthma, the infiltration is usually predominantly neutrophilic.įrom the physiological point of view, acute asthma has two components: an early acute aspect marked by bronchoconstriction that occurs at the smooth muscle level this, bronchoconstriction is usually episodic (asthmatic crisis or exacerbation) and an inflammatory component that develops later and causes edema of the airways. Many inflammatory mediators are involved in this process, including interleukins (IL)-3, IL-4, IL-5, IL-6, IL-8, IL-10, and IL-13, leukotrienes, and granulocyte-macrophage colony-stimulating factors (GM-CSF). The inflammation is generally predominantly eosinophilic, although the involvement of other cells, such as T cells, neutrophils, and mast cells, has also been identified. One of the main triggers for an acute asthma attack is exposure to an allergen, which in susceptible people causes inflammation of the respiratory airways.
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