Scientists redefine arterial wall inflammation

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A specific type of tissue microphage plays a key role in maintaining healthy arteries after inflammation, according to research from the University of Toronto, Canada. Investigators found that this group of tissue macrophages is created, and operates, separately from bone marrow macrophages.

“We’ve discovered that a group of macrophages are created when the embryo is developing, before the bone marrow is functioning,” says 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.”

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

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,” says Robbins, who is also the Peter Munk Chair of Aortic Disease Research in the Toronto General Research Institute at University Health Network, Canada. “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,” says 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.”