Mar. 1, 1999 Washington D.C. - A new study shows how Chlamydia infections may be linked to heart disease. The evidence, presented in the 26 February issue of Science, suggests that Chlamydia employ a sneaky tactic known as "molecular mimicry" that triggers an autoimmune response in the host and ultimately leads to inflammation of the heart.
In the past, several epidemiological studies, which track the occurrence of disease in large populations, have shown an intriguing correlation between Chlamydia infections and heart disease. Until now, however, the mechanism that might link the two has remained a mystery. It is clear that both disorders are significant public health problems. Chlamydia is a primary cause of sexually transmitted diseases and female infertility, and can also cause eye infections and pneumonia in children. Meanwhile, heart disease is the major cause of death in Western societies.
Kurt Bachmaier, of the Ontario Cancer Institute and University of Toronto, and his colleagues in Canada, Austria, and the U.S., now show that the link between Chlamydia infections and heart disease appears to involve what is known as an autoimmune disorder. Like the proverbial wolf in sheep's clothing, some pathogens carry proteins on their surfaces that are almost identical to proteins on the host's cells. These proteins enable the pathogens to evade the host's immune system by "passing" as part of the host's own body. Sometimes, however, the immune system is not fooled by this subterfuge and launches an attack. An autoimmune disorder arises when the attack damages the host's cells in the process.
Bachmaier and his colleagues found that a specific piece of a protein on Chlamydia's surface is a dead ringer for another piece of the protein in the heart muscle of mice known as "myosin." Their findings suggest that a Chlamydia infection, in the lungs or reproductive organs, for example, triggers a local immune response that can be followed by a system-wide activation of the immune system. An autoimmune disorder in the heart occurs when the host's immune cells also direct their attack towards the heart muscle myosin.
Previous studies have shown that injecting mice with this type of myosin resulted in inflammatory heart disease. Bachmaier's group identified the specific section, or peptide sequence, of the myosin molecule that induced the disease. The researchers then screened a public databank for viral and bacterial sequences that matched the myosin peptide sequence. They found matches in peptides from proteins on the outer membranes of three different Chlamydia strains. When the group injected mice with the Chlamydia peptides, these peptides activated the same immune cells as the heart muscle myosin and also induced inflammatory heart disease.
Chlamydia infections are so common that most people can expect to experience at least one during their lifetimes. In the researchers' mouse model, whether or not an infection led to heart disease depended on genetic differences among the various strains of inbred mice. The researchers speculate that genetic and environmental risk factors may also predispose certain humans to Chlamydia-mediated heart disease.
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