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UCSF Team Identifies Two Key Molecules In Asthma; Important Finding For New Therapies That Treat Disease At Cell Level

research is part of ongoing work over the past 20 years by the UCSF Lung Biology Center.

Asthma affects nearly 12.5 million Americans, including 4.8 million children, and the incidence has been rising dramatically in recent years.

People with asthma have airway passages that are chronically inflamed. The inflammation leaves the airways particularly sensitive to allergens, viruses, or environmental factors like dust or tobacco smoke. Exercise, in particular, can trigger an asthma attack, in which the passages constrict and breathing is difficult.

"Current therapies treat only the symptoms of asthma, so with our new understanding we are excited about the possibilities of moving toward treatments that control the disease from its point of origin," said Gabriele Grünig, DVM,PhD, UCSF postdoctoral visiting scientist and principal author of the Science paper.

It is hoped that new treatments also will be able to avoid some of the side effects associated with current therapies, such as water retention in the tissues or a generally depressed immune system.

One scientific theory has proposed that cellular response to the inflammation creates the narrowing of the air passageway, but the UCSF findings show it is the other way around, Grünig said.

The UCSF team found that the molecule/receptor connection initiates the inflammation and also increases the number of a particular type of cell known as a goblet cell, which produces excessive amounts of mucus in the airway passages during an asthma attack.

One interesting aspect of IL-4 and IL-13 is that they appear to be detrimental only in lung tissue. In other parts of the body, they perform good works, according to Corry. In the gut, for example, they play a key role in eliminating parasites and preventing related disease.

UCSF co-investigators on the study team were Rajeev Venkayya, MD; Dean Sheppard, MD; Martha Warnock, MD; Adil E. Wak
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Contact: Corinna Kaarlela
corinna@itsa.ucsf.edu
415-476-3804
University of California - San Francisco
17-Dec-1998


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