title: Enteric microflora contribute to constitutive ICAM-1 expression on vascular endothelial cells.
abstract: Quantitative estimates of endothelial cell adhesion molecule expression have revealed that some adhesion molecules [e.g., intercellular adhesion molecule-1 (ICAM-1)] are abundantly expressed in different vascular beds under normal conditions. The objective of this study was to determine whether the enteric microflora contribute to the constitutive expression of ICAM-1 and other endothelial cell adhesion molecules in the gastrointestinal tract and other regional vascular beds. The dual radiolabeled monoclonal antibody technique was used to measure endothelial expression of ICAM-1, ICAM-2, vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in conventional, germ-free mice and germ-free mice receiving the cecal contents of conventional mice to reestablish the enteric microflora (total association). Constitutive ICAM-1 expression was significantly lower in the splanchnic organs (pancreas, stomach, small and large intestine, mesentery, and liver), kidneys, skeletal muscle, and skin of germ-free mice compared with their conventional counterparts. These differences were abolished after total association of germ-free mice with the indigenous gastrointestinal flora. The expression of ICAM-2, VCAM-1, and E-selectin in the various tissues studied did not differ between conventional and germ-free mice. These findings indicate that the indigenous gastrointestinal microflora are responsible for a significant proportion of the basal ICAM-1 expression detected in both intestinal and extraintestinal tissues.
authors.affiliation: First Department of Surgery, Nagoya University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Komatsu
authors.forename: R D
authors.initials: RD
authors.lastname: Berg
authors.forename: J M
authors.initials: JM
authors.lastname: Russell
authors.forename: Y
authors.initials: Y
authors.lastname: Nimura
authors.forename: D N
authors.initials: DN
authors.lastname: Granger
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis / Q000096:biosynthesis / Q000276:immunology; D002448:Cell Adhesion / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis / Q000276:immunology; D019040:E-Selectin / Q000032:analysis / Q000096:biosynthesis / Q000276:immunology; D004730:Endothelium, Vascular / Q000737:chemistry / Q000378:metabolism* / Q000382:microbiology*; D007082:Ileum / Q000098:blood supply / Q000276:immunology / Q000382:microbiology*; D007113:Immunity, Innate; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis* / Q000276:immunology; D007962:Leukocytes / Q000166:cytology; D008099:Liver / Q000737:chemistry / Q000378:metabolism; D008168:Lung / Q000737:chemistry / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012867:Skin / Q000737:chemistry / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D019040:E-Selectin; C065289:ICAM2 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1