title: Social disruption stress increases IL-6 levels and accelerates atherosclerosis in ApoE-/- mice.
abstract: BACKGROUND
  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.
authors.affiliation: The Wallenberg Laboratory, Department of Molecular and Clinical Medicine/Clinical Physiology, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.
authors.forename: Evelina
authors.initials: E
authors.lastname: Bernberg
authors.forename: Marcus A
authors.initials: MA
authors.lastname: Ulleryd
authors.forename: Maria E
authors.initials: ME
authors.lastname: Johansson
authors.forename: Göran M L
authors.initials: GM
authors.lastname: Bergström
mesh_terms: D000818:Animals; D001018:Aortic Diseases / Q000097:blood / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000523:psychology; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000523:psychology; D054360:Chemokine CXCL1 / Q000097:blood; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D018450:Disease Progression; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D012307:Risk Factors; D012919:Social Behavior; D013315:Stress, Psychological / Q000150:complications*; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D001057:Apolipoproteins E; D054360:Chemokine CXCL1; C475895:Cxcl1 protein, mouse; D018836:Inflammation Mediators; D015850:Interleukin-6; D003345:Corticosterone