The connection between immune function, chronic inflammation, and increased risk for heart disease may have been found; as has a possible way of breaking the connection.
It seems that at least some of the proteins the immune system deploys to “fight germs may also help fat and cholesterol clog our arteries.” This is what “new research” reveals. “Understanding” exactly how this transpires “could eventually lead to new drugs” for arresting the development of heart disease.
From the very inception “of atherosclerosis research almost a hundred years ago,” the possible connection between the condition and the immune system has been noted with the finding of “white blood cells in the fatty plaques on artery walls.” The molecular narrative for this possible connection has, however, eluded researchers; as has the explanation for why it is that diseases marked by chronic inflammation – diseases such as lupus, inflammatory bowel disease, and hepatitis – “increase the risk of high fat and cholesterol levels in patients, which in turn increase the risk of atherosclerosis.”
Finding the answers to these questions is what a team of biochemists at the University of Chicago set out to do. They worked with mice they bred to have “an excess of immune cell molecules called LIGHT” which have been implicated in impairing liver function. Accordingly, they found that mice replete with LIGHT, even though fed a normal diet, “developed cholesterol and fat levels higher than normal mice on high-fat diets.” As might be expected, this pathology only worsened when LIGHT-replete mice were fed high-fat, high cholesterol diets.
Subsequently, the researchers contrived a way to prevent “LIGHT from activating any inflammatory pathways in the mice.” Within several weeks, “mice on the therapy” had their cholesterol and triglyceride levels “returning close to normal.” This result suggests to the researchers “that LIGHT stops the liver from digesting the fatty molecules, forcing them into the bloodstream.”
One of the senior authors of the paper, pathologist Yang Xin Fu, “thinks” the therapy should also work in humans. If so, “the therapy would work through a different mechanism than current statin drugs,” thus affording a new weapon against atherosclerosis.
Others, however, would like more data to be accumulated to see whether or not the LIGHT interdiction really has the effects imputed to it. As immunologist, Luc Teyton, of the Scripps research Institute in San Diego, California, USA, cautions, interventions effected through manipulation of LIGHT are attended by “such broad consequences on development and health,” it may be “that the lipid effects may simply be a by-product of these drastic alterations, not a direct link.”
(Reference: Williams, Sarah C. P. 2007. “The Immune System’s Hardened Truth.” Science. 13 April.)