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Asthma

Description
Asthma is an inflammatory disorder of the airways, characterized by periodic attacks of wheezing, shortness of breath, chest tightness, and coughing. Asthma causes airflow into and out of the lungs to be restricted. When an asthma attack occurs, the muscles of the bronchial tree become tight and the lining of the air passages swells, reducing airflow and producing the characteristic wheezing sound. Mucus production is increased. Asthma attacks can last minutes to days, and can become dangerous if the airflow becomes severely restricted.

Who is at Risk?
In sensitive individuals, asthma symptoms can be triggered by inhaled allergens, such as pet dander, dust mites, cockroach allergens, molds, or pollens. Asthma symptoms can also be triggered by respiratory infections, exercise, cold air, tobacco smoke and other pollutants, stress, food, or drug allergies. Asthma is found in 3-5% of adults and 7-10% of children. Half of the people with asthma develop it before age 10, and most develop it before age 30. Many people with asthma have an individual and/or family history of allergies, such as hay fever or eczema. Others have no history of allergies or evidence of allergic problems. About half of all new cases of asthma in adults over age 40 occur in people who smoke cigarettes and have other lung disease, such as chronic bronchitis or emphysema.

Sources: A.D.A.M., Inc., Healthwise, Incorporated

Mysterious gdT Cells Promote Wound Repair
Diseases like asthma, psoriasis, and ulcerative colitis are all caused by adverse inflammation of their respective epithelial tissues, the outermost layers of the lung, gut, and skin. The key to treating some of these diseases may come from understanding a single type of immune cell that resides mainly in these epithelial tissues - the heretofore mysterious gdT cell ("gamma-delta"). The first major biological role of this cell has been identified by TSRI scientists, led by associate professor Wendy Havran, Ph.D. These cells play a major role in promoting wound repair. They arise early in fetal development in the thymus. From there, they migrate to epithelial tissues. Most gdT cells do not circulate through the bloodstream. Instead, they are the major T cell component of the skin, lung, and intestine, where they take up residence and monitor the neighboring epithelial cells for damage and disease. When wounds heal, the epithelial cells in the skin have to proliferate and fill in the wounds. gdT cells help this proliferation. When skin is cut or damaged, keratinocytes, which are the major type of epithelial cell in the epidermis, are able to faster re-epithelialize tissue that has been wounded if they can get help from the gdT cells.

When gdT cells are missing, there is a delay in wound repair because the wound doesn't have the rapid producers of keratinocyte growth factor right there. Havran's findings should be of interest to doctors who treat diseases that arise from epithelial cell disorders. These findings may eventually lead to the discovery of chemical compounds that could be used to treat conditions like cancer, psoriasis, ulcerative colitis, and asthma. In 1998, some 6.8 million adults in the United States and 3.8 million American children experienced an asthma attack. Knowing the role of these cells in the skin and the mechanism whereby they interact with other skin cells may yield potential targets for intervention in asthma. There is a correlation between asthma and the number of gdT cells in the lungs. During an attack, the number of gdT cells is elevated, which may be the body's attempt to deal with the problem. Treatments that are based on a thorough understanding of the underlying mechanisms of gdT cells may prove to be better than currently existing therapy. Current treatments for asthma include anti-inflammatories like aspirin and corticosteroids, which shut down the response of the abT cells. Havran suspects that this sort of treatment is sub-optimal because it also kills the gdT cells, which are important for tissue repair. Havran hopes the work will lead to new therapeutic agents that spare the gdT cells.

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