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Infectious agents are not necessary for murine atherogenesis
S D Wright1, C Burton, M Hernandez
1Department of Lipid Biochemsitry, Merck Research Laboratories, Rahway, New Jersey 07065, USA. samuel_wright@merck.com
The Journal of Experimental Medicine
|April 19, 2000
Summary
Infection is not required for atherosclerosis development in mice. Studies show that even without microbial agents, the disease progresses similarly, refuting the infectious cause hypothesis.
Area of Science:
- Cardiovascular Science
- Microbiology
- Immunology
Background:
- Correlations between infections and atherosclerotic disease are noted.
- Chlamydia pneumoniae is frequently found in human atherosclerotic lesions.
- This suggests infectious agents may initiate or progress atherosclerosis.
Purpose of the Study:
- To determine if responses to gram-negative bacteria are necessary for atherogenesis.
- To investigate the role of infectious agents in atherosclerosis using germ-free mice.
Main Methods:
- Breeding atherosclerosis-prone apolipoprotein E-deficient (apo E-/-) mice with animals lacking lipopolysaccharide response.
- Creating a colony of germ-free apo E-/- mice, free of all microbial agents.
- Comparing atherosclerosis development in these modified mice with control groups.
Main Results:
- Atherogenesis was unaffected in doubly deficient mice (lacking apo E and LPS response).
- Atherosclerosis in germ-free apo E-/- mice was not measurably different from conventionally raised mice.
- Infection is not necessary for murine atherosclerosis.
Conclusions:
- Infectious agents are not necessary for the initiation or progression of atherosclerosis in mice.
- Koch's postulates cannot be fulfilled for any infectious agent in atherosclerosis.
- Findings challenge the hypothesis that infections are a prerequisite for this disease.