Asthma

Asthma is sometimes referred to as a disease of "twitchy lungs," which means that the airways are extremely sensitive to irritants. The airways are the tubes that bring air from the windpipe, or trachea, to the lungs. These tubes are called the bronchi. Each bronchus, in turn, branches into smaller tubes called bronchioles. At the end of the bronchioles are small, balloon-like structures called alveoli. The alveoli are tiny sacs that allow oxygen to diffuse into the blood and carbon dioxide to diffuse from body tissues into the lungs to be exhaled.

During an asthma attack, the bronchi and bronchioles constrict and obstruct the passage of air into the alveoli. Besides constricting, the airways may secrete copious amounts of mucus in an effort to clear the irritation from the lungs. The airway walls also swell, causing inflammation and further obstruction. As the airways become increasingly obstructed, oxygen cannot reach the small airsacs; blood oxygen levels drop and the body's tissues and organs become oxygen-deprived. At the same time, carbon dioxide cannot escape the small airsacs for exhalation; blood levels of carbon dioxide increase, and exert a toxic effect on the tissues and organs of the body.

Underlying the bronchial inflammation is an immune response in which white blood cells known as type 2 helper T (Th2) cells (a type of CD4 helper T cell) are prominent. Th2 cells secrete chemicals known as interleukins that promote allergic inflammation and stimulate another set of cells known as B cells to produce IgE and other antibodies. In contrast, type 1 helper T (Th1) cells, another class of CD4 T cells, produce interferon-g and interleukin-2, which initiate the killing of viruses and other intracellular organisms by activating macrophages and cytotoxic T cells. These two subgroups of helper T cells arise in response to different immunogenic stimuli and cytokines, and they constitute an immunoregulatory loop: cytokines from Th1 cells inhibit Th2 cells, and vice versa. An imbalance in this reciprocal arrangement may be the key to asthma and there is credible evidence that, when freed from the restraining influence of interferong, Th2 cells can provoke airway inflammation. Recent experiments in support of this concept have focused on a newly discovered transcription factor, T-bet, which is necessary to induce helper T cells to differentiate into Th1 cells and for Th1 cells to produce interferon-g. For these reasons, T-bet is thought to be central to the feedback loops that regulate Th1 and Th2 cells, and in this way it could be important in asthma.

One of the hallmarks of asthma is that the airway obstruction is reversible. This reversibility of the airway swelling is used to definitively diagnose asthma. If the swelling and inflammation can be brought under control with asthma drugs, the person has asthma and not some other upper respiratory tract disease.

In addition to cigarette smoke and various allergens, other triggers can cause asthma attacks. A cold or other upper respiratory infection may bring on an asthma attack. Strong emotions, such as excitement, tension, or anxiety, may trigger asthma symptoms. Exercise can cause symptoms of asthma. Weather conditions, such as extreme cold, heat, or humidity can cause an asthma attack. Pollution and increasing ozone levels are also associated with episodes of asthma. Other environmental factors include occupational exposure to certain substances like animal dander, wood particles, dusts, various industrial chemicals, and metal salts.

The characteristic sign of asthma is wheezing, the noisy, whistling breathing that a person makes as he or she tries to push air in and out of narrowed airways. Other symptoms of asthma include a tight chest, shortness of breath, and a cough.