title: Endotoxin stimulates monocyte-endothelial cell interactions in mouse intestinal Peyer's patches and villus mucosa.
abstract: Although monocyte-endothelial cell interactions represent an initial step in controlling the recruitment of monocytes in inflamed tissues, their dynamic processes in microvessels of lymphoid (Peyer's patches) and non-lymphoid (villus) regions in gut-associated lymphoid tissue remain poorly understood. We monitored the migration of fluorescence-labelled monocytes derived from the spleen in intestinal microvessels with or without lipopolysaccharide (LPS) treatment and investigated the role of adhesion molecules, P-selectin, vascular cell adhesion molecule (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). In control mice, there were few interactions between infused monocytes and the endothelium of intestinal microvessels. The monocyte-endothelial interactions (both rolling and adhesion) were significantly increased in intestinal microvessels of LPS-treated mice compared with those in controls. Anti-P-selectin monoclonal antibody (MoAb) significantly suppressed the LPS-induced increase in monocyte rolling in postcapillary venules of Peyer's patches and submucosal venules. Anti-VCAM-1 MoAbs significantly suppressed the LPS-induced increase in monocyte adhesion to postcapillary venules (PCVs) of Peyer's patches, submucosal venules, and villus capillaries. In contrast, anti-ICAM-1 MoAb significantly suppressed the number of adherent monocytes in PCV of Peyer's patches but not in submucosal venules or villus capillaries. These observations demonstrated that LPS treatment resulted in a significant increase in recruitment of monocytes both in microvessels of lymphoid and non-lymphoid regions and that P-selectin, VCAM-1 and ICAM-1 appeared to play important roles in LPS-induced interactions.
authors.affiliation: Second Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Ishii
authors.forename: Y
authors.initials: Y
authors.lastname: Tsuzuki
authors.forename: K
authors.initials: K
authors.lastname: Matsuzaki
authors.forename: J
authors.initials: J
authors.lastname: Miyazaki
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: R
authors.initials: R
authors.lastname: Hokari
authors.forename: A
authors.initials: A
authors.lastname: Kawaguchi
authors.forename: S
authors.initials: S
authors.lastname: Nagao
authors.forename: K
authors.initials: K
authors.lastname: Itoh
authors.forename: S
authors.initials: S
authors.lastname: Miura
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002448:Cell Adhesion / Q000276:immunology; D042783:Endothelial Cells / Q000276:immunology*; D007150:Immunohistochemistry / Q000379:methods; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000276:immunology*; D019007:P-Selectin / Q000276:immunology; D010581:Peyer's Patches / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D008070:Lipopolysaccharides; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1