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Protein Potentially Links Diet, Obesity, And Asthma

Date:
July 14, 2006
Source:
Journal of Clinical Investigation
Summary:
Australian researchers have identified a new protein -- adipocyte/macrophage fatty acid--binding protein aP2 -- in human airway epithelial cells that regulates allergic airway inflammation in asthma. In addition to its role in type 2 diabetes and atherosclerosis, aP2 is shown to play an essential role in allergic airway diseases, and offers an additional intriguing link between the immune and metabolic systems. The study appears online on July 13 in the Journal of Clinical Investigation.
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Australian researchers have identified a new protein in human airway epithelial cells that regulates allergic airway inflammation. This protein – adipocyte/macrophage fatty acid–binding protein aP2 – is known to regulate the uptake by fat cells of fatty acids and has been previously linked to insulin resistance in diabetes and the development of atherosclerosis.

This new study suggests that in addition to its role in type 2 diabetes and hardening of the arteries, aP2 plays an essential role in allergic airway diseases such as asthma, and offers an additional intriguing link between the immune and metabolic systems. The study will appear online on July 13 in advance of print publication in the August issue of the Journal of Clinical Investigation.

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.


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The above post is reprinted from materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


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Journal of Clinical Investigation. "Protein Potentially Links Diet, Obesity, And Asthma." ScienceDaily. ScienceDaily, 14 July 2006. <www.sciencedaily.com/releases/2006/07/060714083035.htm>.
Journal of Clinical Investigation. (2006, July 14). Protein Potentially Links Diet, Obesity, And Asthma. ScienceDaily. Retrieved July 31, 2015 from www.sciencedaily.com/releases/2006/07/060714083035.htm
Journal of Clinical Investigation. "Protein Potentially Links Diet, Obesity, And Asthma." ScienceDaily. www.sciencedaily.com/releases/2006/07/060714083035.htm (accessed July 31, 2015).

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