Messenger boy here.
The article is a bit confusing.Are they saying that the meds would stop
mucuous production or attacks altogether?
http://www.chron.com/disp/story.mpl/ap/health/3629343.html
"ST. LOUIS - A two-drug treatment may one day help restore healthy
breathing in those with asthma and chronic bronchitis, according to a
study at Washington University in St. Louis.

Dr. Michael Holtzman and other researchers found that some cells lining
the air passages of the lungs transform into another cell type in mice
and humans with those disorders, leading to the overproduction of mucus
in the airways.

Though researchers expect it would take at least a few years for
further testing of the treatments, they think that combining two drugs
ultimately could prevent the harmful transformation of the lining
cells, allowing for healthy airway function.

Holtzman said the findings are "pushing the rock a little further up
the hill" when it comes to understanding airway diseases.

The study appeared Wednesday in the Journal of Clinical Investigation.

Holtzman explained that doctors currently prescribe treatments to ease
breathing difficulties, but said those treatments don't address mucus
production.

Researchers studied mice with a lung condition resembling asthma and
chronic obstructive pulmonary disease, a disease classification that
includes chronic bronchitis.

They saw that the airway lining maintained an overabundance of
mucus-producing cells, called goblet cells because they have a cup-like
shape.

Those goblet cells built up because of two cellular mechanisms. One
mechanism allowed for the prolonged survival of cells with cilia, tiny
hairs that help sweep debris out of the lungs. The other encouraged
those cells to transform into goblet cells.

Holtzman said in some people viral infections or other factors seemed
to cause an excess of goblet cells, leading to certain breathing
disorders. He said the researchers showed that the excess cells could
be blocked, using a combination of two types of inhibitors.

One impedes the activity of a protein called the epidermal growth
factor receptor. The protein is overactive on the ciliated airway cells
in mice with the asthma-like condition. If the protein was blocked, the
inhibitor prevented the buildup of those cells.

The researchers also tested a second inhibitor that interferes with
signaling pathways activated by an immune-system protein known as
interleukin-13. They found that IL-13 brought out the change from
ciliated to goblet cells in mouse airways and human airway cells in
culture. If IL-13 was interfered with, the transformation from one cell
type to the other was prevented.

Holtzman said if the inhibitors are combined, they can "restore the
normal architecture of the airway lining."

Dr. Kenneth Adler, a cell biology professor at North Carolina State
University in Raleigh, said the researchers' work to inhibit cells that
increase mucus was significant, because currently there aren't any
therapies to effectively treat that problem.

"Mice aren't people, and cells in culture aren't airways in people," he
noted. But, he said, if the findings held true in additional studies,
they could be highly significant in treating humans."