Cited by 176Atherosclerosis and Cardiovascular DiseasesCholesterol and Lipid MetabolismAortic Thrombus and Embolism

Infectious Agents Are Not Necessary for Murine Atherogenesis

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Wright, Samuel D., Burton, Charlotte, Hernandez, Melba, Hassing, Heide, Montenegro, Judy, Mundt, Steve, Patel, Sushma, Card, Deborah J. +5 more·2000·The Journal of Experimental Medicine

Abstract

Recent work has revealed correlations between bacterial or viral infections and atherosclerotic disease. One particular bacterium, Chlamydia pneumoniae, has been observed at high frequency in human atherosclerotic lesions, prompting the hypothesis that infectious agents may be necessary for the initiation or progression of atherosclerosis. To determine if responses to gram-negative bacteria are necessary for atherogenesis, we first bred atherosclerosis-prone apolipoprotein (apo) E−/− (deficient) mice with animals incapable of responding to bacterial lipopolysaccharide. Atherogenesis was unaffected in doubly deficient animals. We further tested the role of infectious agents by creating a colony of germ-free apo E−/− mice. These animals are free of all microbial agents (bacterial, viral, and fungal). Atherosclerosis in germ-free animals was not measurably different from that in animals raised with ambient levels of microbial challenge. These studies show that infection is not necessary for murine atherosclerosis and that, unlike peptic ulcer, Koch's postulates cannot be fulfilled for any infectious agent in atherosclerosis.

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References 39 · Cited by 176

Research works printed but not linked: 2

  1. Vogel S. Insights into the genetic and molecular basis of LPS responsiveness and macrophage differentiation Beutler B. Tumor Necrosis Factorsthe Molecules and Their Emerging Role in Medicine 1992 485 513 Raven Press, Ltd. New York
  2. Wright S.D. Innate recognition of microbial lipids Gallin J.I. Snyderman R. InflammationBasic Principles and Clinical Correlates 3rd ed 1999 525 535 Lippincott Williams and Wilkins Philadelphia

Authors
Wright, S. D., Burton, C., Hernandez, M., Hassing, H., Montenegro, J., Mundt, S., Patel, S., Card, D. J., Hermanowski-Vosatka, A., Bergstrom, J. D., Sparrow, C. P., Detmers, P. A., & Chao, Y.-S.
Affiliations
  • Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
  • aDepartment of Lipid Biochemsitry, Merck Research Laboratories, Rahway, New Jersey 07065
Venue
The Journal of Experimental Medicine
Published
2000-04-17
Volume
191
Issue
8
Pages
1437-1442
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2157108473
Cited by
176
References
39
Citations by year
2024: 1 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 10 · 2019: 3 · 2018: 6 · 2017: 6 · 2016: 5 · 2015: 11 · 2014: 7 · 2013: 6 · 2012: 7
FWCI
3.43
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Aortic Thrombus and Embolism
Keywords
atherogenesis, atherosclerosis, Chlamydia pneumoniae, bacterial infection, viral infection, lipopolysaccharide, ApoE-deficient mice, germ-free mice, Gram-negative bacteria, Koch's postulates, infectious agents
MeSH terms
Animals, Apolipoproteins E, Arteriosclerosis, Germ-Free Life, Humans, Infections, Mice, Inbred C57BL, Mice, Transgenic, Chlamydophila pneumoniae, Mice, Knockout, Mice

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