A specific cell type plays a key role in maintaining healthy
arteries after inflammation, researchers have found. It’s a discovery that
could provide treatment options for cardiovascular disease — one of the
leading causes of death in North America.

Researchers from the University of Toronto have found
that a specific cell type plays a key role in maintaining healthy arteries
after inflammation. It’s a discovery that could provide treatment options for
cardiovascular disease — one of the leading causes of death in Canada.

The researchers found that a specific type of tissue
macrophage, a group of white blood cells that defend against infection, are
created and operate separately from other macrophages that come from the bone
marrow. Unlike bone marrow macrophages, these cells live in the outer layer of
the arterial wall, can self-replicate and help to heal the vessel after
inflammation.

“We’ve discovered that a group of macrophages are
created when the embryo is developing, before the bone marrow is
functioning,” said Clinton Robbins, a professor in the Faculty of
Medicine’s Departments of Laboratory Medicine and Pathobiology and Immunology.
“These macrophages can self-replicate and likely regulate the normal
function of our arteries. This is a fundamental biological discovery that could
play an important role in many cardiovascular diseases.”

The journal Nature Immunology published the
results of the study today.

Robbins and his team found that during infection these
self-replicating macrophages leave the arterial wall, while macrophages from
the bone marrow come in and engulf the bacteria. The team thinks that once
inflammation resolves, the self-renewing macrophages return to heal the damaged
tissue.

Using a special tagging system, they accurately traced
where the macrophages were coming from.

“Previously, we couldn’t identify one macrophage
from another because we were limited by technology,” said Robbins, who is
also the Peter Munk Chair of Aortic Disease Research in the Toronto General
Research Institute at University Health Network. “Now we can see exactly
where they’re coming from and where they’re going. Our job now is to get a
better understanding of what these different macrophage populations are
doing.”

Next, the researchers will study how these resident
macrophages interact with their tissue environment and exactly what role they
might play in cardiovascular disease. By understanding the relationship between
the different cell types, they hope to target inflammation caused by infection
or atherosclerosis more effectively.

“We know that while bone marrow macrophages remove
bacteria, they can also cause atherosclerosis by entering the arterial wall and
multiplying,” said Rickvinder Besla, graduate student and co-lead author.
“In the old model, you might try to shut the bone marrow response down,
but this leaves the patient immunosuppressed. Our new model suggests we could
possibly reduce inflammation by boosting the activity of these self-replicating
macrophages.”

Robbins acknowledges that there’s still a lot to learn
about the complexity of these macrophages and how they interact with their
environment and other cells.

“Arteries are more than tubes that shuttle blood
around. They create a complex and dynamic network that reacts to inflammation
and disease in different ways. We’re excited to figure out another piece of
this puzzle and how we might target cardiovascular disease in the future.”

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