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Chlamydia Protein Linked to Heart Disease

Researchers have found a strong piece of new evidence for the theory that infections can cause heart disease. In tomorrow's Science, they report that the Chlamydia pathogen makes a peptide that mimics a portion of a heart muscle protein and triggers a severe inflammation of the heart muscle in mice.

The finding bolsters circumstantial links between infections and heart disease (Science, 3 July 1998, p. 35), including a recent report in the Journal of the American Medical Association that antibiotic use reduces the risk of heart attack. Researchers have been perplexed, however, about how the two might be related. Immunologist Josef Penninger of the Ontario Cancer Institute and colleagues had previously shown that injecting a fragment of the heart muscle protein myosin into mice causes severe inflammatory responses in the animals' hearts. Penninger figured that this intense response to one of the body's own proteins meant the immune system was mistaking the heart peptide for something foreign--perhaps a peptide in a microbe to which the mice had previously been exposed. To come up with a likely suspect, he looked for the offending peptide in protein databases.

The sequence of the myosin fragment closely matched that of a peptide found in three strains of Chlamydia trachomatis, the culprit in the sexually transmitted disease bearing its name. The researchers soon confirmed that injecting Chlamydia peptides into mice provokes heart inflammation, caused by immune system T cells infiltrating the heart muscle. But perhaps the most crucial evidence was the finding that live bacteria pumped into the noses or genital tracts of mice caused subsequent heart inflammation. "Our paper takes this out of the realm of epidemiology and really says this is a causal link," says Penninger. It also implies that preventive treatment with antibiotics might thwart some heart disease cases.

Other researchers say it's far from proven this scenario in mice occurs in people, too. Cardiologist Brent Muhelstein at the University of Utah in Salt Lake City notes that the inflammation seems confined to the mouse heart muscle rather than extending to the arteries, where it could trigger the plaques characteristic of atherosclerosis. Moreover, unlike other strains, C. trachomatis, which evokes the strongest response in Penninger's study, hasn't yet turned up in atherosclerotic plaques.