Kameswara Rao Badri, Phd

American Lung Association Interstitial Lung Disease Scholar

Pulmonary fibrosis is a disease marked by scarring of the tissue inside and between the air sacs in the lungs. When the scar forms, the tissue becomes stiff and thicker. This makes it harder for oxygen to pass through the walls of the air sac into the bloodstream. Once the lung tissue becomes scarred, the damage cannot be reversed.

“I am thankful to the American Lung Association for laying the foundation for my long-term goal of becoming an independent researcher.”
As pulmonary fibrosis develops, an increasing number of connective tissue cells called fibroblasts and myofibroblasts are formed. Myofibroblasts are cells with characteristic features of both fibroblasts and smooth muscle cells. These cells are important in wound repair responses and tissue remodelling. In pulmonary fibrosis, too many fibroblasts and myofibroblasts accumulate in lung as a result of different cellular events, depositing large amounts of collagen and producing excessive scarring. TGF-ßI plays a central role in these cellular events and represents the most powerful fibrosis promoting growth factor identified so far. Fibroblasts and myofibroblasts are activated by TGF-ßl.

With the help of an American Lung Association Dalsemer Research Grant, Dr. Badri is investigating the role of a molecule called P311 that regulates TGF-ßl expression. He will determine whether the lack of P311 in mice will protect against development of the disease. He will induce IPF in the mice using a drug called bleomycin. “Molecules that regulate TGF-ßI will regulate activated fibroblasts and myofibroblasts,” Dr. Badri says. “Any molecule that regulates TGF-ßI and the numbers of activated fibroblasts and myofibroblasts is definitely of interest for the treatment of pulmonary fibrosis. So it is important to find a target, such as P311, that controls TGF-ßl levels.” The ultimate goal, he says, is to reduce the number of fibroblasts and myofibroblasts through the regulation of different molecular mechanisms associated with the development of IPF. Dr. Badri adds that research involving mouse aortas has shown that P311 also regulates vascular contraction, so it may also be involved in hypertension. “This means our findings may also have implications for other lung diseases that involve the pulmonary blood vessels,” he says.

“I am thankful to the American Lung Association for laying the foundation for my long-term goal of becoming an independent researcher in this field,” he notes. “This funding will also allow me to gather data which will permit me to submit proposals for federal funding.”