title: Splenectomy increases atherosclerotic lesions in apolipoprotein E deficient mice.
abstract: BACKGROUND
  Atherosclerosis is an inflammatory immune disease associated with lipid accumulation in the intima layer of arteries. The spleen plays an important immune function, but its influence in development of atherosclerosis remains unclear. Evaluation of the role of the spleen in atherosclerosis is justified due to the high frequency of total splenectomies. In this work, the effect of splenectomy on the development of atherosclerosis in apolipoprotein E (ApoE) deficient mice was investigated.
  
  
  METHODS
  ApoE deficient mice were divided into a sham-operated control group (CT) and a splenectomized group (SP). Thirty days after surgery, animals were fed a high fat western diet. After 8 wk, mice were euthanized and their blood, heart, and aorta were subjected to analysis. Atherosclerotic lesion areas in the aortic root were stained with hematoxylin-eosin and quantified by morphometry. The atherosclerotic lesions in the thoracic and abdominal portions of aorta were determined by assessing the percentage of the luminal surface area stained by Sudan IV. Total serum cholesterol and anti-oxidized LDL antibodies were measured.
  
  
  RESULTS
  Levels of total serum cholesterol did not vary significantly after splenectomy. Anti-oxidized LDL IgG antibodies were similar between groups. However, compared with the control group, lesions in the aortic root were significantly larger in splenectomized mice (P<0.01). These data were confirmed by the increase of atherosclerotic area in the thoracic and abdominal portions of aorta in splenectomized mice.
  
  
  CONCLUSIONS
  These data indicate that splenectomy increases atherosclerotic lesions in ApoE deficient mice fed an atherogenic diet, suggesting an atheroprotector role of the spleen.
authors.affiliation: Department of Morphology, Institute of Biological Sciences, Federal University of Juiz de Fora, Juiz de Fora, Brazil.
authors.forename: Alice B
authors.initials: AB
authors.lastname: Rezende
authors.forename: Náira N
authors.initials: NN
authors.lastname: Neto
authors.forename: Luciana R
authors.initials: LR
authors.lastname: Fernandes
authors.forename: Ana Cecília C
authors.initials: AC
authors.lastname: Ribeiro
authors.forename: Jacqueline I
authors.initials: JI
authors.lastname: Alvarez-Leite
authors.forename: Henrique C
authors.initials: HC
authors.lastname: Teixeira
mesh_terms: D000818:Animals; D001018:Aortic Diseases / Q000235:genetics / Q000503:physiopathology; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000235:genetics* / Q000503:physiopathology*; D001323:Autoantibodies / Q000097:blood; D001835:Body Weight / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D004036:Diet, Atherogenic; D004435:Eating / Q000502:physiology; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D013154:Spleen / Q000502:physiology* / Q000601:surgery; D013156:Splenectomy / Q000009:adverse effects*
chemical_list: D001057:Apolipoproteins E; D001323:Autoantibodies; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D002784:Cholesterol