Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE−/− mice
Abstract
Introduction
We have previously shown that different forms of stress have distinctive effects on atherogenesis in mice. We showed that social stress increase atherosclerosis in ApoE−/− mice, while more physical forms of stress do not. Here we evaluated the effect of social disruption (SDR) stress on atherogenesis and evaluated cytokine release after SDR-stress and five more physical stressors.
Methods
Male ApoE−/− mice were exposed to SDR-stress during 12
weeks, and atherosclerotic plaque area was assessed in aorta, aortic root and innominate artery. Further, male C57BL/6 mice were exposed to SDR-stress or five physical stressors, and cytokine and corticosterone levels were analyzed in plasma/serum samples immediately after stress.
Results
We found a correlation between the level of SDR-stress and atherosclerotic plaque area in aorta and a numerical increased plaque area in aortic root. SDR stress did not affect histological features of plaque composition. However, SDR-stress increased levels of corticosterone, IL-6 and CXCL1. Plasma corticosterone increased for all five physical stressors, but IL-6 and CXCL1 only increased in the group exposed to restraint combined with rat odor.
Conclusions
These findings suggest that SDR-stress is indeed atherogenic, in contrast to our previous results using the physical stressors. A possible explanation to this difference is that SDR-stress, but not physical stressors, leads to release of the pro-inflammatory cytokines IL-6 and CXCL1.
Keywords: Atherosclerosis, Social disruption stress, ApoE−/− mice, IL-6, CXCL1, Physical stressors
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PII: S0021-9150(11)01113-0
doi:10.1016/j.atherosclerosis.2011.11.041
© 2011 Elsevier Ireland Ltd. All rights reserved.
