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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Toll-like receptor 4 polymorphisms and atherogenesis.

Stefan Kiechl1, Eva Lorenz, Markus Reindl

  • 1Department of Neurology, University Clinic, Innsbruck, Austria. stefan.kiechl@uibk.ac.at

The New England Journal of Medicine
|July 19, 2002
PubMed
Summary

Genetic variants in toll-like receptor 4 (TLR4) influence inflammatory responses. The Asp299Gly TLR4 variant is linked to reduced atherosclerosis risk, suggesting innate immunity

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Area of Science:

  • Immunology
  • Cardiovascular Disease Research
  • Genetics

Background:

  • Innate immunity, while protective against pathogens, may increase atherosclerosis risk.
  • Toll-like receptor 4 (TLR4) genetic variants affect inflammatory responses to bacterial lipopolysaccharide.
  • Investigating the link between TLR4 variants and atherosclerosis development is crucial.

Purpose of the Study:

  • To determine if specific genetic variants of toll-like receptor 4 (TLR4) are associated with the development of atherosclerosis.
  • To explore the relationship between TLR4 polymorphisms and inflammatory markers related to cardiovascular disease.

Main Methods:

  • Screened 810 participants in the Bruneck Study for TLR4 polymorphisms (Asp299Gly and Thr399Ile).
  • Assessed carotid atherosclerosis extent and progression using high-resolution duplex ultrasonography.
  • Measured levels of proinflammatory cytokines, acute-phase reactants, and soluble adhesion molecules.

Main Results:

  • Subjects with the Asp299Gly TLR4 allele showed lower levels of interleukin-6 and fibrinogen.
  • Despite increased susceptibility to severe bacterial infections, these subjects had a significantly lower risk of carotid atherosclerosis (OR=0.54, P=0.05).
  • A smaller intima-media thickness in the common carotid artery was observed in subjects with the Asp299Gly variant (P=0.01).

Conclusions:

  • The Asp299Gly TLR4 polymorphism, which reduces inflammatory response to pathogens, is associated with decreased atherosclerosis risk.
  • This supports the hypothesis that innate immunity plays a role in the pathogenesis of atherosclerosis (atherogenesis).
  • Targeting inflammatory pathways mediated by TLR4 could offer new strategies for atherosclerosis prevention.