CHICAGO, June 7 (Xinhua) -- Researchers at Washington University School of Medicine in St. Louis have zeroed in on B cells that try to heal the injured heart following a heart attack but instead trigger inflammation that leads to even more damage.

The study is published June 7 in JCI Insight.

And they also found that an already approved drug, Pirfenidone, effectively tamps down such inflammation in mice, protecting the heart from the progressive damage that often occurs after a heart attack.

The researchers' immune studies of the heart still focus on other types of immune cells, including macrophages, T cell lymphocytes, neutrophils and monocytes. They first did not find any differences in the numbers of such immune cells in the injured hearts of mice that received pirfenidone versus those that didn't. But when they serendipitously measured B cells, they saw a huge difference.

"Our results showing B cells driving heart inflammation was quite unexpected," said first author Luigi Adamo, a clinical fellow in cardiology. "We didn' t know that B cells have a role in the type of heart damage we were studying until our data pushed us in that direction. We also found that there isn't just one type of B cell in the heart, but a whole family of different types that are closely related. And pirfenidone modulates these cells to have a protective effect on heart muscle after a heart attack."

When these cells were removed completely, not only was the heart not protected, the beneficial effect of the drug went away. So the B cells are not exclusively bad, the researchers said.

"The protective effects of pirfenidone hinge on the presence of B cells," Adamo said. "The drug may be working on other cells as well, perhaps directly or perhaps through the B cells. We're continuing to investigate the details."

Pirfenidone, a drug approved by the Food and Drug Administration to treat a lung condition called idiopathic pulmonary fibrosis, has long been considered safe. But it can have such side effects as nausea and vomiting.

Now that the researchers have identified B cell lymphocytes as the drug's target, they can begin investigating ways to make it better.