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Inflammation Protein Linked to Asthma

By HospiMedica staff writers
Posted on 02 Aug 2006
A protein previously linked to the development of type 2 diabetes and atherosclerosis may also be associated with asthma, a new study has suggested.

A team of Australian and American researchers has found a protein called aP2 in the lining of the human lung, where it appears to regulate the inflammation associated with asthma. More...
The protein has no useful function in the body, and only appears during the course of disease. It seems to cause adverse effects on blood sugar levels and fatty acid metabolism, and has previously been found in fat cells and macrophages in obese people and those with diabetes or heart disease. The study was published in the July 13, 2006, online issue of the Journal of Clinical Investigation.

In mice with an animal model of asthma, the researchers found that aP2 regulated the infiltration of inflammatory molecules into the lungs, suggesting that there is a link between the metabolic and immune systems. To study the effects of aP2, the researchers created genetically engineered mice that could not produce the protein.

"They're metabolic supermice,” said study co-author Dr. Gokhan S. Hotamisligil, of the Harvard School of Public Health (Boston, MA, USA). "We cannot make them obese, diabetic, or atherosclerotic. They don't develop fatty liver disease, and they don't develop asthma.”

Pharmaceutical companies have developed aP2-blocking drugs to treat diabetes and atherosclerosis, but the researchers think the new study may spur the development of versions that could be used to treat asthma, since it can be administered locally into the airways. Because the linings of the lungs only have 1/10,000 th as much aP2 as fat cells do, in theory, it would require much less medication to inhibit the protein. Human trials of aP2-blocking drugs probably will not be held for another three or four years.

"The exciting thing about this study is that perhaps the way all of these diseases are connected is through the inflammatory responses controlled by this boring little protein,” concluded Dr. Hotamisligil.



Related Links:
Harvard School of Public Health

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