New research clears the way to healing lung disease

Senior author on the paper, Associate Professor Katrina Binger from the Department of Biochemistry and Molecular Biology at Monash University, created a 3D tissue culture system that mimics the fibrotic environment and identified vitronectin as being critical in switching the macrophages to cause scarring rather than healing.  

“We normally think of vitronectin as a structural protein that maintains the integrity of organs like the lungs. But we found it also can also act as a signal,” she said. 

“Vitronectin changes how macrophages produce energy, and this drives them to have a heightened fibrotic state. This is a completely new mechanism to understand how fibrosis happens that was only possible by studying these cells in more natural, 3D environments.”

“Importantly, what we saw in our 3D cultures was perfectly mirrored by animal models run by Associate Professor Liu’s team and in tissue samples from patients with IPF.”

The next step for the team is to identify new treatments that can use the vitronectin-macrophage pathway to treat IPF.  

“Understanding this mechanism is critical to identifying new therapeutic agents for fibrosis patients,” Associate Professor Liu said. 

“Now we can work to identify new drugs that can most effectively inhibit vitronectin so we can translate this research into clinical practice and help find a new cure for this debilitating disease.”