Microparticles could reduce heart attack damage
Less achy breaky Biodegradable microparticles could dramatically reduce the inflammatory damage that occurs during a heart attack, potentially making the difference between life and death.
The study, conducted on mice, found that the microparticles significantly reduced the amount of scarring in the heart tissue and promoted repair.
The serendipitous discovery was made by an international team of researchers using poly (lactic-co-glycolic) acid microparticles to track an immune cell called an inflammatory monocyte.
These cells are a primitive 'first responder' to the site of inflammation, cleaning up dead or dying cells. Unfortunately, they often cause more damage by releasing enzymes and chemicals that also kill off living cells.
"Although the principle behind these inflammatory monocytes is almost certainly one of cleaning up the debris … in heart attack situations, they often come in great floods and do a lot more damage when the blood flow is re-established," says co-author Professor Nicholas King, Professor of Immunopathology and head of the Department of Pathology at the University of Sydney.
The team noticed that whenever they injected the microparticles, which are ingested by the monocytes, they failed to turn up at the site of the inflammation.
Further investigation revealed that the monocytes changed after ingesting the microparticles.
"They seem to change their phenotype - in other words what they appeared to be and what they appeared to function as - and they started expressing markers on the cell surface that suggest to the body that they are actually dying," King says.
So instead of heading to the site of inflammation, the monocytes were captured by the spleen, which filters out unhealthy or dying cells from the blood stream.
"What we seem to have discovered is that by using this natural pathway we actually prevent these cells from going into the focus of inflammation and that reduces the inflammation fantastically."
"It doesn't catch them all, but it catches most."
Researchers then applied this to the mouse model of a heart attack, and discovered significant improvements.
"We can reduce the scarring by up to 50 per cent, which is quite substantial, and it increases the functional output of the heart by something like 30 per cent," says King.
"If you reduced the amount of damage to the heart muscle, then you could in fact save them."
Researchers are now hoping to test the approach in humans, but say that in theory, it could be applied to any disease with an inflammatory component, such as rheumatoid arthritis and even cancer.
The results are published today in the journal Science Translational Medicine.