Current hypothesis states that airway inflammation may be acute, subacute, or chronic. The acute response is determined by early recruitment of cells to the airway. Antigens come in contact with mast cells in the submucosa and cause elaboration of mediators, such as histamine, leukotrienes (including leukotriene B 4), chemokines, tryptase, interleukin 5 (IL-5), IL-8, proinflammatory cytokines, and IL-4, which produce an intense inflammatory reaction, with bronchoconstriction, vascular congestion, edema formation, increased mucus production, and impaired mucociliary transport. Eosinophils, platelets, and polymorphonuclear leukocytes are recruited to the site, activated, and contribute further to the inflammatory cycle that has already been initiated. The immunoglobulin E (IgE) response is controlled by T and B lymphocytes and activated by the interaction of antigen with the mast cell-bound Ig-E molecules.9 In the subacute or late phase, recruited and resident cells are activated, causing a more persistent pattern of inflammation.
Chronic inflammation is characterized by a persistent cell damage and an ongoing repair process, contributing to some of the microscopic changes seen in the airway. Mediators target ciliated airway epithelium to cause injury or disruption. As a consequence, epithelial cells and myofibroblasts, present beneath the epithelial layer, proliferate and begin to deposit interstitial collagen in the lamina reticularis of the basement membrane. Fibroblasts contribute to the process by releasing cytokines and chemokines, which may be important in both initiating and maintaining the level of airway inflammation and may explain the apparent basement membrane thickening and irreversible airway changes seen in some asthmatics.10 Clearly, the inflammatory process is multicellular, redundant, and self-amplifying.
Allergic asthma is frequently associated with a personal or family history of allergic diseases such as rhinitis, urticaria, and eczema. Idiosyncratic, or nonallergic, asthma is associated with no family history or personal history of allergy and normal serum levels of IgE. Many stimuli have been noted to provoke an increase in airway responsiveness. Viral respiratory infections are the most common of the stimuli that invoke acute asthma exacerbation.11 Increased airway responsiveness secondary to infection may last anywhere from 2 to 8 weeks.11 Exercise is another common precipitant of acute asthma. Unlike other precipitants of acute exacerbation, long-term sequelae and airway reactivity are not noted as a result of exercise. Environmental conditions, such as atmospheric pollutants and antigens noted in heavy industrial or densely populated urban areas, are associated with higher incidence and severity of asthma. In addition, indoor antigens such as mold, house dust mites, cockroaches, and animal dander, are also associated with acute asthma. Occupational exposures, such as metal salt, wood and vegetable dust, pharmaceutical, industrial chemical and plastic, biological enzyme, vapors, gases, and aerosol, may also stimulate an asthma attack. Multiple pharmaceutical agents, such as aspirin, b blockers (including topical b blockers), nonsteroidal anti-inflammatory agents, sulfating agents, tartrazine dyes, and food additives and preservatives have been implicated in acute asthma. As in exercise-induced asthma, exposure to cold air alone can induce acute bronchospasm. Recent evidence indicates that endocrine factors, such as changing levels of estradiols and progesterone during the normal menstrual cycle and pregnancy, may contribute to the level of airway reactivity.1 I3 Finally, emotional stress can produce an asthma attack.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.