Atheromatosis, which lies behind heart attacks, stroke, and other cardiovascular problems, has a major impact on public health. So does chronic rheumatoid arthritis.
These two diseases are completely different from each other, but they do have one common denominator: inflammation. Researchers at Lund University in Sweden can now show that it might also be possible to treat them with the same drug.
Chronic rheumatoid arthritis (RA) is a result of inflammation of the joints. Inflammation is actually the body´s way of dealing with infections caused by bacteria, but in rheumatoid arthritis the immune system overreacts, attacking the body´s own tissues.
Inflammation is also involved in atherosclerosis (also called hardening of the arteries). When fat is stored in blood vessels and becomes rancid, the body tries to rid itself of the fat by calling in so-called inflammatory cells, white corpuscles. But the reaction is often too powerful, so the inflammatory cells start to break down the walls of the vessels in the same way they break down joint cartilage and bone in rheumatoid arthritis.
A central role in inflammation in rheumatoid arthritis is played by a signal molecule called TNF-alpha. Heart scientist Stefan Jovinge can now show that TNF-alpha is also involved in atheromatosis/atherosclerosis. His research team first developed a special breed of mice that was prone to develop this disease, whereupon they knocked out the gene for TNF-alpha and found that the mice developed less atheromatosis/atherosclerosis.
The same result was achieved by giving these atheromatosis-conditioned mice a drug that impedes the effect of TNF in the body. The findings have recently been published in the journal “Arteriosclerosis, Thrombosis and Vascular Biology”.