Infectious Agents Are Not Necessary for Murine Atherogenesis
Open accessAbstract
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.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Germ-free atherogenic mice lacking apolipoprotein E show a worsening of atherosclerotic lesions after being fed a high-cholesterol diet compared with conventionally raised mice.
“the germ-free atherogenic mice lacking apolipoprotein E (Apoe -/ ) mice, which are without the colonization of gut microbiota, show a worsening of atherosclerotic lesions after being fed a high-cholesterol diet compared with the conventionally raised mice”
From <i>Akkermansia Muciniphila</i> Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in <i>Apoe</i> <sup>−/−</sup> Mice (2016) · cites this paper as [15]
Antibiotic therapy fails to elicit any beneficial effect on cardiovascular events in human trials.
“antibiotic therapy fails to elicit any beneficial effect on cardiovascular events in human trials.[14][15][16]”
From <i>Akkermansia Muciniphila</i> Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in <i>Apoe</i> <sup>−/−</sup> Mice (2016) · cites this paper as [15]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 39 · Cited by 176
Research works printed but not linked: 2
- 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
- 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
- Publisher
- Rockefeller University Press
- Published
- 2000-04-17
- Volume
- 191
- Issue
- 8
- Pages
- 1437-1442
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2193142
- 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
- bronze
- doi.org
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review