McMaster’s research team discovers new mechanism of action for PGX-YBG
PGX-YBG demonstrates ability to reprogram macrophages on its own
PGX-YBG may be a suitable therapeutic solution for patients with fibrotic lung disease and late stage COVID-19 patients
The project, entitled “PGX-processed yeast beta-glucans as an inhalable immunomodulating therapeutic for COVID-19 patients,” jointly funded by
This project was initiated in
“We have shown that the PGX technology can convert materials that can’t easily be inhaled, in particular, a YBG-based particle that has inherent immunomodulatory properties, into materials that can readily access the lung,” commented
The team has successfully demonstrated that Ceapro’s PGX technology can produce low density, highly porous, and purified YBG microparticles with a small and uniform size distribution. These unique particles were found to possess improved aerodynamic properties, allowing them to be inhaled and deposited in the deep lung where fibrotic development occurs.
At the heart of this project is fibrosis: the unregulated and excessive production of scar tissue in organs. Key immune cells called macrophages apparently play a crucial role in maintaining and progressing the fibrotic state. “M1” macrophages express pro-inflammatory properties and “M2” macrophages express the complete opposite anti-inflammatory properties. During fibrosis, M2-like macrophages persist in the fibrotic lung and secrete cytokines (cell signaling molecules) that stimulate the cells around them to constantly produce and deposit scar tissue in the deep lung. These recent findings indicate that PGX-YBG, which binds specifically to Dectin-1 receptors at the surface of macrophages, can repolarize or “reprogram” M2-like macrophages into M1-like macrophages thereby putting an end to tissue deposition (fibrosis) and initiating the much-needed removal of excess tissues.
“We have shown, in vitro, that PGX-YBG have the ability to prevent the activation of macrophages toward a pro-fibrotic phenotype. In addition, PGX-YBG treatment to macrophages that have already acquired a pro-fibrotic phenotype result in the reprogramming of the macrophages toward a classical phenotype not known to be pro-fibrotic. Using cells from animals lacking the beta-glucan receptor Dectin-1, we showed that this was dependent on the presence of the Dectin-1 receptor. These findings are very exciting as macrophage reprogramming is seen as a viable therapeutic strategy toward fibrotic disease and PGX-YBG seem to have this ability. In vivo, we have shown that PGX-YBG can be safely administered to mice, and preliminary data shows an ability to prevent fibrogenesis in an experimental model of lung fibrosis. We are looking forward to validating these in vivo findings over the next few months,” reported
To advance this promising technology to human clinical trials, the Company is working to ensure that the delivery of PGX-YBG to the lung is optimized. It will also be important to further validate PGX-YBG’s performance for reducing lung fibrosis, both alone and loaded with an anti-inflammatory drug currently used for lung fibrosis and COVID-19 therapy. The potential impact of this project is considerable since, one of the most common and deadly fibrotic diseases is IPF for which there are no cure and a short (3-5 year) survival rate. It was recently also shown that lung fibrosis can occur and persists for months in some COVID-19 patients thereby suggesting that COVID-19 survivors may suffer from post-infection pulmonary fibrosis complications.
“We are very pleased with the progress made in this research project. Considering these recent, exciting findings, we believe it certainly becomes necessary to conduct additional animal studies before initiating human trials to develop the best possible tool in the fight against lung fibrotic diseases including COVID-19 and post COVID-19 complications,” commented
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