Atherosclerosis
Volume 221, Issue 2 , Pages 359-365, April 2012

Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE−/− mice

  • Evelina Bernberg

      Affiliations

    • The Wallenberg Laboratory, Department of Molecular and Clinical Medicine/Clinical Physiology, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden
  • ,
  • Marcus A. Ulleryd

      Affiliations

    • Dept. of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden
  • ,
  • Maria E. Johansson

      Affiliations

    • Dept. of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden
  • ,
  • Göran M.L. Bergström

      Affiliations

    • The Wallenberg Laboratory, Department of Molecular and Clinical Medicine/Clinical Physiology, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden
    • Corresponding Author InformationCorresponding author at: Department of Molecular and Clinical Medicine/Clinical Physiology, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden. Tel.: +46 31 342 8011; fax: +46 31 8276 14.

Received 10 April 2011; received in revised form 8 November 2011; accepted 16 November 2011. published online 30 January 2012.

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 12weeks, 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

Atherosclerosis
Volume 221, Issue 2 , Pages 359-365, April 2012