text: Absence of microbiota (germ-free conditions) accelerates the atherosclerosis in ApoE-deficient mice fed standard low cholesterol diet.
  AIM:
  The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice.
  METHODS:
  The experiments were performed on ApoE-/--deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3-4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods.
  RESULTS:
  Conventionally reared ApoE-/- mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE-/- mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls.
  CONCLUSION:
  In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE-/- mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE-/- mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development.
  
entities.text: ['lesions']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T1
entities.text: ['thoracic']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T2
entities.text: ['abdominal aorta']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T3
entities.text: ['aorta']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T5
entities.text: ['atherosclerotic aortic plaques']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T4
entities.text: ['atherosclerotic plaques']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T6
entities.text: ['cells']
entities.type: Cell
entities.entity_id: PMID-20379054_T7
entities.text: ['macrophages']
entities.type: Cell
entities.entity_id: PMID-20379054_T8
entities.text: ['arterial walls']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T9
entities.text: ['atherosclerotic plaques']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T10
entities.text: ['atherosclerotic plaques']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T11
entities.text: ['aorta']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T12
entities.text: ['atherosclerotic plaques']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T13
entities.text: ['atherosclerotic lesions']
entities.type: Pathological_formation
entities.entity_id: PMID-20379054_T14
entities.text: ['intestinal']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T15
entities.text: ['intestinal']
entities.type: Multi-tissue_structure
entities.entity_id: PMID-20379054_T16