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Interleukin-6 exacerbates early atherosclerosis in mice
S A Huber1, P Sakkinen, D Conze
1Department of Pathology, University of Vermont, Burlington, VT 05405, USA. shuber@salus.uvm.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|October 16, 1999
Summary
Interleukin-6 (IL-6) injections promoted atherosclerosis development in mice, suggesting that inflammation, not just a marker, actively contributes to early cardiovascular disease lesion formation.
Area of Science:
- Cardiovascular biology
- Immunology
- Atherosclerosis research
Background:
- Acute-phase proteins and proinflammatory cytokines like interleukin-6 (IL-6) are elevated in cardiovascular disease.
- Elevated levels predict future ischemic events, hinting at a role in early lesion development.
Purpose of the Study:
- To investigate the role of IL-6 and acute-phase proteins in the early stages of atherosclerosis.
- To determine if IL-6 directly influences lesion development in susceptible mouse models.
Main Methods:
- Mice (C57Bl/6, nonobese diabetic, and ApoE-deficient) were fed high-fat diets and injected weekly with recombinant IL-6 (rIL-6) or saline.
- Plasma was analyzed for cytokines, acute-phase proteins (fibrinogen, albumin), and cholesterol.
- Aortic sinus sections were stained to quantify fatty streak lesion size.
Main Results:
- rIL-6 injection significantly increased plasma IL-6, IL-1beta, TNF-alpha, and fibrinogen, while decreasing albumin.
- Total cholesterol levels remained unchanged between groups.
- rIL-6 treatment increased lesion size 1.9- to 5.1-fold in C57Bl/6 and ApoE-deficient mice, but not in nonobese diabetic mice.
Conclusions:
- Changes in circulating proinflammatory cytokines and acute-phase proteins can actively participate in early atherosclerosis development.
- IL-6 plays a causal role in promoting lesion formation under specific conditions.
- This highlights the potential of targeting inflammation in preventing cardiovascular disease progression.