Abstract by Rebecca Viazzo
Chemistry and Biochemistry
Pam Van Ry
avB6 Inhibitor Improves Idiopathic Pulmonary Fibrosis Outcomes
Idiopathic Pulmonary Fibrosis (IPF) is an interstitial lung disease that causes lung fibrosis leading to ineffective oxygen exchange to the blood. Once diagnosed, IPF is fatal within 3-5 years. There is no known cause or treatment that improves outcomes. Although the cause is unknown, it is speculated that the TGFB cell signaling pathway is responsible for the chronic inflammation and fibrosis characteristic of IPF. avb6 integrin is an upstream activator of the TGFB pathway and a therapeutic target. We prove that our avB6 inhibitor, AG2, halts fibrosis in the standard IPF mouse model that uses bleomycin to induce fibrosis in lungs. Fibrosis progression is evaluated through quantifying weekly uCT scans and Masson-Trichrome stained lung sections. Lung sections and uCT scans show lung fibrosis is significantly lower in bleomycin-plus-AG2-treated mice as compared to mice treated with bleomycin alone. This suggests AG2 is a promising therapeutic to improve outcomes of IPF patients.