Cellular pathophysiology of asthma. Top, Cross-section of the normal airway and the asthmatic airway. Mediators released during the inflammatory process associated with asthma cause bronchoconstriction, mucus secretion, and mucosal inflammation and edema. These changes reduce the size of the airway lumen and increase resistance to airflow, which leads to wheezing and shortness of breath. Bottom, The multitude of inflammatory cells (macrophages, eosinophils, mast cells, neutrophils) and neurotransmitters implicated in asthma pathophysiology.
manner in which the disease is treated. Thus, it is useful to discuss the involvement of various mediators and inflammatory cells in antigen-induced asthma, an extensively studied, albeit simplistic, model of the disease. In this model, antigens, such as ragweed pollen or house mite dust, sensitize individuals by eliciting the production of antibodies of the immunoglobulin (Ig) E type. These antibodies attach themselves to the surface of mast cells and basophils. If the individual is reexposed to the same antigen days to months later, the resulting antigen-antibody reaction on lung mast cells will trigger the release of histamine and the cysteinyl leukotrienes, agents that produce bronchoconstriction, mucus secretion, and pulmonary edema. Mast cells also release a variety of chemotactic mediators, such as leukotriene B4 and cytokines. These agents recruit and activate additional inflammatory cells, particularly eosinophils and alveolar macrophages, both of which are also rich sources of leukotrienes and cytokines. Ultimately, repeated exposure to antigen establishes a chronic inflammatory state in the asthmatic airway.
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