Scientists have zeroed in on a type of immune cell that tries to heal the injured heart following a heart attack but instead triggers inflammation that leads to even more damage.
Pirfenidone — a drug approved to treat an unrelated lung condition — was found to work by regulating in the heart the specific response of B cell lymphocytes — the immune cells responsible for the inflammation.
In the study, mice — that modelled human heart attacks — lived longer if they were given pirfenidone.
“Our results showing B cells driving heart inflammation was quite unexpected,” said lead author Luigi Adamo, a clinical student at the Washington University School of Medicine in US.
“We didn’t know that B cells have a role in the type of heart damage. 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,” Adamo added.
In a heart attack, blood is cut off from an area of the heart that then often dies. If the person survives, the body tries to heal the dead muscle by forming scar tissue — but such tissue can further weaken the heart.
However, when well-intentioned immune cells try to heal the injured heart, they instead drive inflammation, further causing damage.
When the researchers removed B-cells completely, the heart was not protected, and the beneficial effect of the drug also went away. So the B cells are not exclusively bad, Adamo 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.
“If we understand how pirfenidone works to reduce inflammation, we can work to modify the drug or make an even better drug that may be able to help a large number of patients,” the researchers noted. IANS
