HARDENED arteries and heart attacks may be the price we pay for fighting
infection. Researchers in Austria have shown that a wide variety of microbes can
trigger an autoimmune reaction against the cells lining our arteries.
Cardiovascular disease is the biggest killer in Western countries. As we age,
our arteries often become clogged up with fatty deposits called plaques. This
narrows the artery, leading to strokes or heart attacks.
It was thought that atherosclerosis鈥� furring of the arteries鈥攚as
simply caused by high cholesterol, or damage to the arteries. More recently, it
has emerged that the disease begins when the artery walls become inflamed. This
could be caused by an infection, raising the intriguing possibility that you can 鈥渃atch鈥� heart disease
(New 杏吧原创, 23 October 1999, p 11).
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But now it seems that rather than a single pathogen being responsible, a
whole host of bugs may be involved. This month, Stephen Epstein of Washington
Hospital Center in Washington DC told a meeting of the European Atherosclerosis
Society in Geneva that the more chronic infections you have, including the
viruses hepatitis A, herpes and cytomegalovirus, and the bacteria Chlamydia and
Helicobacter, the more likely you are to have atherosclerosis. And Edward
Abinader of the Technion in Haifa, Israel, reported that heart attack patients
have often just had sore throats.
Epstein suspects the pathogens boost levels of the immune chemicals that
cause inflammation, making arterial walls vulnerable to plaque. Georg Wick of
the University of Innsbruck in Austria goes further. He thinks the pathogens鈥�
鈥渉eat shock proteins鈥� trigger an autoimmune reaction to human heat shock
proteins.
Heat shock proteins, or HSPs, protect enzymes from damaging stresses, and are
similar in viruses, bacteria and humans. Stresses such as high blood pressure,
smoking and increased cholesterol levels trigger the production of HSPs in cells
in artery walls. When this happens, our immune reaction against pathogens鈥� HSPs
makes us attack our own arteries, says Wick. The effect increases as damage from
arterial stress and immune reactions accumulates with age.
He has shown that immunising rabbits with bacterial HSP produces plaques,
while suppressing inflammation prevents this. Plaques have also been found to
contain immune cells that target HSP. And a long-term study in Italy has shown
that people with more antibodies to HSP have more atherosclerosis and heart
attacks.
Both Wick鈥檚 and Epstein鈥檚 theories suggest atherosclerosis will be hard to
prevent. Six trials are under way to see if treating Chlamydia infection
prevents atherosclerosis. But if a whole host of bugs are involved in the
disease, this approach seem destined to fail.
鈥淢aybe someday a specific anti-inflammatory treatment will be possible,鈥�
Epstein says. 鈥淏ut we can鈥檛 block all inflammation because we need it to fight
infections, and we can鈥檛 stop all these infections.鈥�
鈥淭his is the downside of our ability to fight infections when we are young,鈥�
he adds. 鈥淓volution doesn鈥檛 care if we live so long [our immune system] starts
attacking our arteries as well.鈥�