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The Problem

The incidence of asthma in the United States (as well as in many other developed countries) has reached epidemic proportions. In the last two decades, the number of sufferers in the U. S. has doubled to more than 14 million people.

In an attack of asthma, the bronchi become constricted, making it difficult to breathe in and — especially — out. The sufferer wheezes and coughs. Severe attacks can be life-threatening.

The Mechanism

An attack of asthma begins when an allergen is inhaled. The allergen binds to IgE antibodies — those that have binding sites for the allergen — on mast cells in the lungs. Binding triggers exocytosis of the mast cells with the release of These substances Although asthma begins as an allergic response, in time attacks can be triggered by nonspecific factors like cold air, exercise, and tobacco smoke.

Why do some people develop asthma from exposure to agents that are harmless to others?

For reasons that are not yet understood, some people have a predisposition to respond to antigens by making antibodies of the IgE class. The trait tends to run in families suggesting a genetic component. These people are said to suffer from atopy.

The T helper cells of atopic people are largely of the Th2 type rather that Th1.

And mice whose genes for a transcription factor (called "T-bet") used to make Th1 cells have been knocked out

Th2 helper cells
Link to discussion of Th1 and Th2 cells

Why is asthma a disease of developed countries?

No one knows for certain.

It is certainly not a matter of air pollution. Air pollution can trigger attacks of asthma, but some regions with heavily-polluted air have a much lower incidence of asthma than regions with relatively clean air.

One intriguing possibility: sanitation and widespread childhood immunization may enable children to avoid the infections — especially viral — that stimulate the immune system to respond with Th1 helper cells rather than Th2 cells. Children in Europe that give positive DTH responses to tuberculin (a response mediated by Th1 cells) have lower rates of asthma than children who are negative in the tuberculin test. European children growing up on farms where they are exposed to high levels of bacteria and fungi associated with farm animals have a lower incidence of asthma and atopy than their suburban peers.

But children in tropical, undeveloped countries, who are often infected with parasitic worms, have high levels of Th2 cells and IgE but a very low incidence of asthma. Perhaps, then, a variety of chronic infections in childhood activate mechanisms (e.g., production of regulatory T cells) that suppress all inflammatory immune responses both Th1- and Th2-mediated.


Beta-adrenergic agonists


Cromolyn sodium

Cromolyn sodium (disodium cromoglycate)

Leukotriene inhibitors

Two types of leukotriene inhibitors received FDA approval in 1996.

Possible future treatments still under investigation

Some of these treatments are already in clinical trials. [Discussion of how new drugs are tested]

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27 January 2014