THE shadowy role of bacteria in heart disease is starting to emerge into the
light. New research suggests that bacteria trigger damage to the
arteries鈥攂ut only when the body鈥檚 arsenal of anti-inflammatory chemicals
fails. The news will dampen some scientists鈥� hopes that antibiotics might help
prevent the disease.
快猫短视频s have long suspected that some bacteria, such as Chlamydia
pneumoniae, play a part in causing heart disease
(快猫短视频, 8 June 1996, p 38).
C. pneumoniae has been cultured from the fatty
plaques that build up in patients鈥� arteries, restricting the blood supply to the
heart.
But sometimes plaques from patients contain no traces of suspect microbes.
Nor has anyone explained how bacteria might cause the condition. Alain Tedgui of
INSERM, the French National Institute of Health and Medical Research in Paris,
and his colleagues wondered if the bugs might play an indirect role by altering
the balance of inflammatory chemicals within artery walls.
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To test this, the team fed a diet rich in fat and cholesterol to mice
genetically unable to produce interleukin 10 (IL-10), an anti-inflammatory
chemical normally secreted inside arterial plaques. Even in a sterile
environment, mice without IL-10 developed plaques three times as large as those
in mice with IL-10. And in a nonsterile environment containing typical bacteria
and pollutants, mice lacking IL-10 grew plaques 30 times as large as those in
mice protected by the anti-inflammatory protein.
When the researchers injected genes for IL-10 into the deficient mice, the
animals developed much smaller plaques (Circulation Research, vol 85, p 1).
鈥淭his clearly indicates a causal role for IL-10,鈥� Tedgui concludes.
The scientists think some microbes and certain pollutants can trigger an
inflammatory reaction, which would normally be quenched by anti-inflammatory
chemicals such as IL-10. But individuals whose immune cells produce too many
inflammatory chemicals or too few anti-inflammatory ones may develop
life-threatening plaques.
This suggests that antibiotics would be unlikely to be useful in preventing
heart disease. But the result also hints that anti-inflammatory drugs could be
effective.
David Grainger, a cell biologist at the University of Cambridge, thinks
understanding inflammation is the next challenge for cardiovascular researchers.
鈥淎fter a decade of concentration on cholesterol, I think this is the coming
trend,鈥� he says. 鈥淒iscoveries like this will be seen as milestones.鈥�
But making the leap from mice to people is not simple, warns Margaret
Hammerschlag, who studies Chlamydia at the State University of New York
in Brooklyn. 鈥淚t鈥檚 a fascinating finding,鈥� she says. 鈥淏ut the question always
is, since it鈥檚 a mouse, what鈥檚 the relevance in humans?鈥�
Tedgui acknowledges that mice are not perfect models for human heart disease.
鈥淭he plaques we saw weren鈥檛 as fully evolved as in humans,鈥� he says. And in
animals, arterial plaques never rupture鈥攐ne of the major causes of heart
attacks in people. Tedgui hopes that other researchers will study
atherosclerosis in people with differing levels of IL-10 due to genetic
variation.