Researchers have found that the link between chlamydial infections and heart disease involves an autoimmune response in the infected host.
According to a study published in the journal Science (1999;283:1335-8), researchers from the University of Toronto have discovered that a surface protein on the chlamydia bacterium mimics a peptide found in mouse myosin. This “molecular mimicry” allows the bacteria to invade the mouse without necessarily triggering an immune response in the host. However, the researchers observed that sometimes the host's immune system does recognise the bacteria as “foreign” and, in addition to triggering an immune response against the bacteria, the host mouse begins to attack its own myosin. This results in inflammatory heart disease.
Earlier research had suggested that inflammatory heart disease arises when autoantibodies are produced against the host's own myosin. In order to confirm this, purified myosin peptides were injected into mice. This was found to result in severe heart disease.
In the latest set of experiments, Dr Kurt Bachmaier and his colleagues identified the myosin peptide region responsible for inducing the autoimmune response as a 14 amino acid sequence. They searched databases of known viral and bacterial peptide sequences to see if they could find a match for the mouse myosin peptide. “To our amazement,” said Dr Bachmaier, “we found similarity in the outer membrane of chlamydia bacteria.”
To test their discovery, the researchers injected the chlamydia peptides into mice and confirmed that the same immune cells (CD4 T cells) were activated as when the myosin peptide had been injected. Up to 88%of the mice subsequently developed inflammatory heart disease.