However, thanks to the infusion of money made possible by the American Recovery and Reinvestment Act (ARRA) of 2009, NIAID was able to fund both of Dr. Tsoukas’s projects.
“We were aware of the extremely high competition for NIH funds,” says Dr. Tsoukas. “Without ARRA funds, the lab would probably have been forced to close down.”
The funds have allowed Dr. Tsoukas to focus on his research. In addition, the funds support graduate students who are just starting their professional careers. Two students in existing positions had faced an unwelcome choice: find a new laboratory position and start over from scratch or discontinue their degrees. Thanks to ARRA funding, they have been able to continue their work in Dr. Tsoukas’s lab, joined by three new graduate students whose positions also are supported by ARRA.
The graduate students will be able to complete the research required for their Ph.D. and M.S. degrees and possibly move on to postdoctoral, academic, or industry positions as highly trained specialists.
“This new funding is providing support to develop these young scientists whose future work will benefit society and the economy many times over the initial, relatively small investment provided by ARRA,” says Dr. Tsoukas.
In addition to creating jobs, funding laboratory research increases demand for supplies, instrumentation, and equipment maintenance, which benefits science support industries that provide technical expertise and other goods and services. It also holds tremendous promise for improving public health.
Dr. Tsoukas’s lab focuses on bronchial asthma, a debilitating disease that affects millions of people worldwide. Unfortunately, the majority of today's treatments take care of the symptoms and not the cause of the disease.
His lab studies a protein called ITK, which regulates the production of cytokines—a type of chemical in the immune system that under normal circumstances protects the body from infections. However, in some individuals cytokines may cause bronchial asthma in response to certain environmental irritants. In order for ITK to work and mediate the production of cytokines, including those that cause asthma, it must interact with another molecule known as SLP-76.
The lab is manipulating the gene that makes ITK by changing it at strategic locations. Then they test whether that change makes ITK inactive or over-reactive. They also are devising methods to inhibit the interaction of ITK and SLP-76.
“We believe that our work will lead to better understanding of how ITK works and how it is involved in bronchial asthma,” says Dr. Tsoukas. “We also feel that it will provide a platform for the design of novel drugs that will prevent this disease.”
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Last Updated November 02, 2009