Toll-Like Receptors found to trigger stroke and heart disease

Research lead

Researchers at Imperial College London have shown that the Toll-like receptor TLR-2, which initiates the body’s immune response against pathogens, is central to the development of atherosclerosis.

In atherosclerosis, plaques made of fatty deposits and cholesterol form inside arteries. Immune cells are attracted into these plaques, leading to the artery becoming inflamed and the artery wall being damaged. The new research shows that TLR-2 is unusually active in plaques in the carotid artery in the neck. In lab tests, the researchers showed that blocking the TLR-2 receptor stopped the inflammatory cascade. They also suggest that this means bacterial infections may be involved in triggering atherosclerosis by switching on the TLR-2 molecules.

Claudia Monaco, of the Kennedy Institute of Rheumatology and Vascular Surgery at Imperial College, said, “Our new study reveals the trigger for inflammation and tissue breakdown in artery plaques. We have also shown that this trigger mechanism can be blocked using antibodies.”

The researchers studied sections of the carotid artery with atherosclerosis, taken from 58 patients after a stroke. They used enzymes to break down the artery tissue to a suspension of single cells. After four days the cells produced an unusually large volume of inflammatory cytokines and artery-damaging enzymes.

It was subsequently shown that blocking TLR-2 using an antibody reduced the production of inflammatory molecules and enzymes dramatically.