About 50 percent of all deaths in the United States can be attributed to atherosclerosis. Atherosclerosis is a disease of the arteries in our bodies. It is currently believed that some sort of injury occurs to the cells lining the arteries. These cells are called endothelial cells. Platelets (cells that help to repair blood vessel damage) and white blood cells (monocytes) then adhere to the area that is damaged. Factors released from the monocytes and platelets attract smooth muscle cells to the site of the damage. Smooth muscle cells are close by and are what cause our blood vessels to get smaller (constrict) and get larger (dilate).
The smooth muscle cells multiply and produce collagen, fibrin, elastic fibers, and proteoglycans (a protein with a long chain(s) of sugars attached to it). Collagen, fibrin, elastic fibers, and the proteoglycans help to hold the whole damaged area together into what is called an atheroma (Normal artery). Meanwhile, the monocytes go inside the atheroma and become macrophages that can produce large amounts of fatty substances (lipids). These lipids are mostly cholesterol and cholesterol esters (cholesterol with another fatty substance (fatty acid) bound to it).
Short-lived damage does not usually result in an atheroma. However, long-term or chronic damage is usually what causes an atheroma to eventually form. These atheromas take literally years to form and may actually have started when a person is quite young.
These atheromas get larger and larger. If an artery that gives nutrients and oxygen to the heart (coronary artery) is clogged, a heart attack (mycardial infarction) can occur. That is why people are often tested to determine the amount of blockage that exists in these coronary arteries. No blood to the heart muscle and it starts dying off. No pumping of blood and our bodies indeed get very ill very quickly. Atheromas can occur most anywhere in our bodies and can result in damage to our brains, feet and hands and can cause our vessels to expand like a balloon (aneurysm).
A recent article in Infection and Immunity has provided more evidence that a bacterium called Chlamydia pneumoniae may be one of those causes of chronic damage to our endothelial cells. Previous investigators have been able to show that people with atherosclerosis are very likely to produce antibodies to Chlamydia pneumoniae. They have also been able to isolate Chlamydia pneumoniae from an atheroma. Chlamydia pneumoniae can live inside endothelial cells and damage them once inside the cells. The researchers in the current article demonstrated that Chlamydia pneumoniae can cause endothelial cells to produce factors that bring these monocytes to the endothelial cells.
Chlamydia pneumoniae can live for long periods of time in the
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