Asthma is a chronic inflammatory disorder of the airway involving many different types of cells and cellular elements. The chronic inflammation leads to an increase in airway hyperresponsiveness with recurrent episodes of wheezing, coughing, and shortness of breath. Inflammation is evident, even in patients with intermittent asthma.2 Airflow limitation is widespread, variable, occurs throughout the tracheobronchial tree, and is usually reversible spontaneously or with treatment. However, if poorly controlled, it can be irreversible. Airway remodeling is a long-term consequence of inflammation, but early treatment limits the damage from inflammation, and inhaled corticosteroids (ICS) suppress inflammation. read only
Asthma is a chronic airway disorder characterized by hyperreactivity to various stimuli, airway inflammation, bronchospasm, and airway obstruction. Triggers of asthma include antigens, viruses, pollutants, and occupational agents. These triggers stimulate an inflammatory cascade involving many cells and mediators. This cascade is complex and interactive and varies between patients, within individual patients and with age, but leads to inflammation, bronchial hyperreactivity, airflow obstruction, and symptoms of asthma. The small airways, with internal diameters of < 2 ^m, are major sites of inflammation and airway obstruction.- These sites are characterized by frequent hypertrophy of airway smooth muscle, new vessel formation, increased numbers of epithelial goblet cells, and deposition of interstitial collagen beneath the epithelium; these morphologic changes may not be completely irreversible.
These changes, which occur with chronic inflammation, are involved in remodeling of the airways, which is discussed more fully later in this article. Mucus plugging causes further constriction of the airway lumen. The effects of long-term asthma on lung function were shown in the Copenhagen City Heart Study, in which a sample of male nonsmokers in the general population who identified themselves as having asthma had substantially greater declines in FEV1 over time than those who did not have asthma (Fig 1).
Figure 2 shows the inflammatory cascade involved in airway inflammation. The inflammatory process of asthma appears to involve mast cells, eosinophils, epithelial cells, macrophages, and activated T-cells, which can influence airway function through secretion of preformed and newly synthesized mediators that act directly on the airway or indirectly through neural mechanisms.
Figure 1. Changes in FEV1 with the presence or absence of asthma in male nonsmokers in the Copenhagen City Heart Study. Reproduced with permission.
Figure 2. The inflammatory cascade in asthma. Reproduced with permission from the National Asthma Education and Prevention Program.6 LTB-4 = leukotrience B4.