title: Lymphocyte recruitment and the kinetics of adhesion receptor expression during the pulmonary immune response to particulate antigen.
abstract: The selectins and beta2 integrins participate in the recruitment of neutrophils in acute pulmonary inflammation. However, the cell adhesion receptors that mediate lymphocyte trafficking into the lung have not been defined. This study examined the relationship between cell adhesion molecules on the pulmonary vasculature and on lymphocytes recovered from the lung during a pulmonary immune response to intratracheal (I.T.) sheep red blood cells (SRBCs) in sensitized C57BL/6J mice. Silver-enhanced immunogold staining and reverse transcriptase polymerase chain reaction of lung tissues revealed sustained induction of VCAM-1, E-selectin, and P-selectin on the pulmonary vasculature for up to 7 days after I.T.-SRBC challenge. Neither the MECA 79 nor MECA 367 antigens were induced on the pulmonary vasculature during this period. In the peripheral blood, both CD4 and CD8 T-cell subsets showed an initial increase in P-selectin ligand expression after I.T.-SRBC challenge. The number of P-selectin ligand-positive T cells in the peripheral blood fell as T cells with both P-selectin and, to a lesser extent, E-selectin ligands accumulated in the bronchoalveolar lavage fluid. We conclude that I.T.-SRBC challenge in sensitized mice elicits prolonged synthesis of P-selectin, E-selectin, and VCAM-1 by the lung vasculature as well as selectin ligand synthesis by responding T cells. Furthermore, the entry of selectin-ligand-positive T cells into the circulation and their accumulation in the bronchoalveolar lavage fluid indicates that these receptors may contribute to T cell recruitment. Finally, VCAM-1 on the vasculature may also participate; however, the vascular addressins, required for homing to peripheral and mucosal lymphoid organs, are not essential for T-cell entry into the lung following I.T.-SRBC challenge.
authors.affiliation: Department of Pathology, University of Michigan Medical Center, Ann Arbor 48109-0602, USA.
authors.forename: F M
authors.initials: FM
authors.lastname: Wolber
authors.forename: J L
authors.initials: JL
authors.lastname: Curtis
authors.forename: A M
authors.initials: AM
authors.lastname: Milik
authors.forename: T
authors.initials: T
authors.lastname: Fields
authors.forename: G D
authors.initials: GD
authors.lastname: Seitzman
authors.forename: K
authors.initials: K
authors.lastname: Kim
authors.forename: S
authors.initials: S
authors.lastname: Kim
authors.forename: J
authors.initials: J
authors.lastname: Sonstein
authors.forename: L M
authors.initials: LM
authors.lastname: Stoolman
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000096:biosynthesis; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D016516:CD4-CD8 Ratio; D017931:DNA Primers / Q000737:chemistry; D019040:E-Selectin / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004912:Erythrocytes / Q000276:immunology; D005260:Female; D007700:Kinetics; D008565:Membrane Proteins; D051379:Mice; D008810:Mice, Inbred C57BL; D019007:P-Selectin / Q000096:biosynthesis*; D011014:Pneumonia / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D016133:Polymerase Chain Reaction; D016201:Receptors, Lymphocyte Homing / Q000096:biosynthesis; D013047:Specific Pathogen-Free Organisms; D013601:T-Lymphocytes / Q000502:physiology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis*
chemical_list: D000954:Antigens, Surface; D017931:DNA Primers; D019040:E-Selectin; C069886:L-selectin counter-receptors; D008565:Membrane Proteins; D019007:P-Selectin; D016201:Receptors, Lymphocyte Homing; D019010:Vascular Cell Adhesion Molecule-1