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The Alpha-1 Foundation Awards Two Research Grants with Support from Talecris Biotherapeutics, Inc.

Posted Oct 14 2009 10:01pm

images The Alpha-1 Foundation announced today that it has awarded two research grants to study how genetic variations in the alpha-1 antitrypsin (AAT) gene contribute to lung and liver damage in people with AAT deficiency. The inherited condition causes emphysema and liver disease. The research will also investigate whether AAT infusion therapy — known as augmentation therapy — minimizes liver damage among individuals with AAT deficiency.

The grants were awarded to Noel G. McElvaney, M.D., professor in the Department of Medicine, Royal College of Surgeons, Dublin, Ireland, and to Cristy Lee Gelling, Ph.D., in the Department of Biological Sciences at the University of Pittsburgh.

The grants were made possible through an unrestricted charitable donation from Talecris Biotherapeutics to the Alpha-1 Foundation.

“Scientific research will enable us to better understand the processes by which the disease damages the lungs and liver,” said Steve Petteway, Ph.D., executive vice president, Research and Development, at Talecris Biotherapeutics. “Our ultimate goal is to improve the lives of individuals with AAT deficiency by developing safe and effective therapies.”

AAT deficiency occurs when the liver produces insufficient levels of AAT protein or misshapen AAT proteins. In healthy individuals, AAT helps regulate the activity of white blood cells (known as neutrophils) in the lungs. Once the neutrophils have cleared debris and damaged cells in the lungs, they are neutralized or inactivated by AAT. In the absence of sufficient AAT, neutrophils continue to attack lung tissue, leading to lung tissue destruction. AAT infusions help prevent the excessive activity of neutrophils in the lungs.

Research studies

McElvaney’s research will examine how infusions of AAT reduce the levels of destructive molecules known as reactive oxygen species (ROS). ROS are produced by neutrophils circulating in the lungs. AAT inhibits the activity of neutrophils and thus the production of ROS. When AAT is deficient, ROS levels rise dangerously and inflict damage to lung tissue. McElvaney’s team will study how infusions of AAT bind to neutrophils.

Gelling’s research will investigate which variants of the alpha-1 antitrypsin gene predispose individuals with AAT deficiency to liver damage and which gene variants are protective. Researchers have previously shown that individuals with the “Z” mutation of AAT gene are at increased risk for producing sticky AAT proteins that clump in the liver and form plaques. Yet scientists have no way of predicting which individuals will be affected. Gelling’s team will use genetically engineered baker’s yeast to produce the sticky proteins and then analyze precisely how the proteins malfunction.

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