Heart immune cell discovery

31 October 2014 

Researchers from St Louis’s Washington School of Medicine have discovered that the heart can recover from injuries using its own immune cells. Their findings, which were observed in mice, have been published in The Proceedings of the National Academy of Sciences Early Edition.

The research could lead to improved treatments in human cardiology patients, since the experiments were designed to mirror the conditions of cardiac failure

Previous studies had already established that a neonatal mouse heart can regrow its lower tip when it is cut off, whereas an adult mouse heart will merely form scar tissue. Previously, it was thought that the same immune cells, known as macrophages, were responsible for the damage in the adult heart and the neonatal regeneration, making it impossible to explain the phenomenon.

However, new research by the same team, led by Douglas L. Mann, Tobias and Hortense Lewin Professor of Medicine and cardiologist-in-chief at Barnes-Jewish Hospital, has shed light on the reasons for the differences.

The study has been able to identify the difference between macrophages from the bone marrow, which increase the inflammation and damage in the adult tissue, and the heart’s macrophages, which bring about the growth and repair in the younger tissue.

In adult tissue, the macrophages that promote healing are present, but they appear to be overwhelmed by immune cells from the bone marrow after an injury takes place. This may account for the disparity in recovery prospects.

It is possible to distinguish between heart and bone marrow macrophages by the presence of a protein called CCR2 on the cell surface. Immune cells from bone marrow have this protein, whereas those from the heart do not.

The researchers then investigated whether the presence of a substance that inhibited the CCR2 protein would prevent the damaging bone marrow macrophages from entering injured heart tissue. This led to an improved recovery in the damaged adult tissue.

The research’s first author Kory J. Lavine said: “When we did that, we found that the macrophages from the bone marrow did not come in, the macrophages native to the heart remained. We saw reduced inflammation in these injured adult hearts, less oxidative damage and improved repair.” The research’s conclusion is that the CCR2 inhibitors preserved the heart macrophages, and thus improved the recovery prospects.

Interestingly, some CCR2 inhibitors are in stage one and two clinical trials for the treatment of rheumatoid arthritis. However, there is some way to go before the substances can begin clinical trials for treating heart disease.

Lavine and his colleagues have identified research into the subtypes of macrophages present in the human heart as their next priority. While there are similarities between mouse and human heart immune cells, the functions of those found in humans have not yet been proven.

It is not known, for example, whether immune cells from the human heart have the same healing properties as the corresponding macrophages in mice. The role played by bone marrow immune cells in human heart failure must also be conclusively established.

Posted by Jeanette Royston​


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