Washington, USA (ISJ) – Latest research at Washington University School of Medicine in St. Louis shows, heart holds its own pool of immune cells capable of helping it heal after injury.
Normally when the heart is injured, these beneficial immune cells are supplanted by immune cells from the bone marrow, which are spurred to converge in the heart and cause inflammation that leads to further damage. Both these immune cells are called macrophages – be it from the heart or in the bone marrow. Its origin determines whether it is helpful or harmful to an injured heart.
Research shows, in a mouse model of heart failure, blocking the bone marrow’s macrophages from entering the heart protects the organ’s beneficial pool of macrophages. The macrophages in the heart promote regeneration and recovery. This finding may have implications for treating heart failure in humans.
“Researchers have known for long time that the neonatal mouse heart can recover well from injury, and in some cases can even regenerate,” said the lead author of the study Kory J. Lavine, instructor in medicine. “If you cut off the lower lip of the neonatal mouse heart, it can grow back. But if you do the same thing to an adult mouse heart, it forms scar tissue.”
Until recently, it was impossible to distinguish the helpful macrophages that reside in the heart from the harmful ones that arrive from the bone marrow.
The new research and research in the past by the group led by Douglas L. Mann, the Tobias and Hortense Lewin Professor of Medicine and cardiologist-in-chief at Barnes-Jewish Hospital, appear to implicate these immune cells of different origins as responsible for the difference in healing capacity in neonatal and adult heart, at least in mice.
“The same macrophages that promote healing after injury in the neonatal heart also are present in the adult heart, but they seem to go away with injury,” Lavine said. “This explains why young heart can recover while the adult heart can’t.”
Lavine and his colleagues developed a method to progressively damage mouse cardiac tissue in a way that mimicked heart failure. They compared the immune response to cardiac damage in neonatal and adult mouse hearts.
The researchers found, the helpful macrophages originate in the embryonic heart and harmful ones in the bone marrow and could be distinguished by a protein on their surface called CCR2. Macrophages without CCR2 originate in the heart while those with CCR2 come from the bone marrow, the study showed.