The "hygiene hypothesis" currently dominates thinking in the medical field about the underlying causes of asthma. The hypothesis proposes that childhood infection and environmental factors such as diet and airborne pollution contribute to a predisposition to this condition. Michael Rolph and colleagues from The Garvan Institute of Medical Research, Sydney, now show for the first time that the protein aP2 is present in human epithelial cells lining the tubes that carry air from the windpipe to the lungs (bronchi), and that aP2 expression is significantly increased when these cells are stimulated with the molecules interleukin-4 and –13. This finding is very unexpected as aP2 has previously been considered to be a specific marker for fat cells. The group went on to show that mice lacking aP2 have a dramatic reduction in airway inflammation in a model of asthma. In addition, the infiltration into the airways of inflammatory molecules such as leukocytes and eosinophils was highly dependent on aP2 function in mice. The data emphasize the importance of lipids in the inflammatory response and contribute to the emerging theme that an overlap exists between the pathways that regulate inflammation and those that govern metabolism. Finally, the study suggests that blocking aP2 function may be a novel approach for the treatment of asthma and other inflammatory lung diseases.
TITLE: The adipocyte fatty acid–binding protein aP2 is required in allergic airway inflammation
Michael S. Rolph
The Garvan Institute of Medical Research, Sydney, NSW, Australia.
Phone: 61-2-9295-8531; Fax: 61-2-9295-8404; E-mail: firstname.lastname@example.org.
Gokhan S. Hotamisligil
Harvard School of Public Health, Boston, Massachusetts, USA.
Phone (617) 432-1950; Fax: (617) 432-1941; Email: email@example.com.
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Last reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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