Fig. 14.13 Histologic evidence of chronic inflammation in the airways of an asthmatic patient. Panel a shows a section through a bronchus of a patient who died of asthma; there is almost total occlusion of the airway by a mucus plug. In panel b, a close-up view of the bronchial wall shows injury to the epithelium lining the bronchus, accompanied by a dense inflammatory infiltrate. Although not discernable at this magnification, the infiltrate includes eosinophils, neutrophils, and lymphocytes. Photographs courtesy of T. Krausz.
clinically as seasonal allergic rhinoconjunctivitis) is caused by a variety of allergens, including certain grass and tree pollens. Symptoms in the late summer or autumn are commonly caused by weed pollen, such as that of ragweed, or the spores of fungi such as Alternaria. Ubiquitous allergens such as Fel d 1 in cat dander, Der p 1 in the feces of house dust mites, and Bla g 1 in cockroach can be a cause of year-round, or perennial, allergic rhinoconjunctivitis.
A more serious IgE-mediated respiratory disease is allergic asthma, which is triggered by allergen-induced activation of submucosal mast cells in the lower airways. This can lead within seconds to bronchial constriction and an increased secretion into the airways of fluid and mucus, making breathing more difficult by trapping inhaled air in the lungs. Patients with allergic asthma usually need treatment, and severe asthmatic attacks can be life threatening. The same allergens that cause allergic rhinitis and conjunctivitis commonly cause asthma attacks. For example, respiratory arrest caused by severe attacks of asthma in the summer or autumn has been associated with the inhalation of Alternaria spores.
Chronic allergen exposure leads to an important feature of asthma, namely, chronic inflammation of the airways, which is characterized by the continued presence of increased numbers of pathologic lymphocytes, eosinophils, neutrophils, basophils, and other leukocytes (Fig. 14.13). The concerted actions of these cells cause airway hyperreactivity and remodeling—a thickening of the airway walls due to hyperplasia and hypertrophy of the smooth muscle layer, with the eventual development of fibrosis. Fibrotic remodeling leads to a permanent narrowing of the airways, and is responsible for many of the clinical manifestations of chronic allergic asthma. In chronic asthmatics, a general hyperreactivity of the airways to nonimmunological stimuli such as perfumes or volatile irritants also often develops.