title: Eosinophil tissue recruitment to sites of allergic inflammation in the lung is platelet endothelial cell adhesion molecule independent.
abstract: Platelet endothelial cell adhesion molecule (PECAM or CD31) is a cell adhesion molecule expressed on circulating leukocytes and endothelial cells that plays an important role in mediating neutrophil and monocyte transendothelial migration in vivo. In this study, we investigated whether eosinophils, like neutrophils and monocytes, utilize PECAM for tissue recruitment to sites of allergic inflammation in vivo. Eosinophils express similar levels of PECAM as neutrophils as assessed by FACS analysis. RT-PCR studies demonstrate that eosinophils like neutrophils express the six extracellular domains of PECAM. Eosinophils exhibit homophilic binding to recombinant PECAM as assessed in a single-cell micropipette adhesion assay able to measure the biophysical strength of adhesion of eosinophils to recombinant PECAM. The strength of eosinophil adhesion to recombinant PECAM is the same as that of neutrophil binding to recombinant PECAM and can be inhibited with an anti-PECAM Ab. Although eosinophils express functional PECAM, anti-PECAM Abs did not inhibit bronchoalveolar lavage eosinophilia, lung eosinophilia, and airway hyperreactivity to methacholine in a mouse model of OVA-induced asthma in vivo. Thus, in contrast to studies that have demonstrated that neutrophil and monocyte tissue recruitment is PECAM dependent, these studies demonstrate that eosinophil tissue recruitment in vivo in this model is PECAM independent.
authors.affiliation: Department of Medicine, University of California at San Diego, La Jolla, CA 92093, USA.
authors.forename: M
authors.initials: M
authors.lastname: Miller
authors.forename: K L
authors.initials: KL
authors.lastname: Sung
authors.forename: W A
authors.initials: WA
authors.lastname: Muller
authors.forename: J Y
authors.initials: JY
authors.lastname: Cho
authors.forename: M
authors.initials: M
authors.lastname: Roman
authors.forename: D
authors.initials: D
authors.lastname: Castaneda
authors.forename: J
authors.initials: J
authors.lastname: Nayar
authors.forename: T
authors.initials: T
authors.lastname: Condon
authors.forename: J
authors.initials: J
authors.lastname: Kim
authors.forename: P
authors.initials: P
authors.lastname: Sriramarao
authors.forename: D H
authors.initials: DH
authors.lastname: Broide
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001772:Blood Cell Count; D001854:Bone Marrow Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology; D002448:Cell Adhesion / Q000276:immunology; D002465:Cell Movement / Q000276:immunology*; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005110:Extracellular Space / Q000276:immunology / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007106:Immune Sera / Q000008:administration & dosage; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007274:Injections, Intraperitoneal; D008168:Lung / Q000276:immunology* / Q000473:pathology*; D016210:Methacholine Chloride / Q000008:administration & dosage; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis / Q000276:immunology / Q000502:physiology*; D017434:Protein Structure, Tertiary; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D007106:Immune Sera; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D016210:Methacholine Chloride