title: Organism-specific neutrophil-endothelial cell interactions in response to Escherichia coli, Streptococcus pneumoniae, and Staphylococcus aureus.
abstract: The recruitment of polymorphonuclear leukocytes (PMNs) from the vascular space into the lung interstitium and airspace is an early step in the host innate immune response to bacterial invasion of these sites. To determine the ability of intact bacteria to directly elicit PMN migration across an endothelial monolayer, we studied in vitro migration of PMNs across a monolayer of human pulmonary microvascular endothelial cells in response to Streptococcus pneumoniae, Staphylococcus aureus, and Escherichia coli, as well as to purified E. coli LPS. Bacterial induction of PMN migration was dose dependent and elicited by > or =10(4) bacteria/ml of each of the species tested. Pretreatment of PMNs with blocking Abs to CD18 significantly inhibited migration of PMN in response to all stimuli tested, but had the most profound effect on migration to S. pneumoniae and S. aureus. Intact E. coli were 10 times more potent in inducing transmigration of PMNs than a corresponding amount of purified LPS. Bacterial induction of PMN migration did not correlate with up-regulation of surface endothelial ICAM-1 expression (purified LPS >> intact E. coli > S. aureus and S. pneumoniae) nor up-regulation of VCAM-1 and E-selectin. Neutralizing Ab to ICAM-1 had no effect on PMN migration to any of the bacteria or to purified LPS. These findings demonstrate that diverse bacterial pathogens induce PMN migration across a pulmonary microvascular endothelial cell monolayer in a fashion that appears to be organism specific. In addition, intact bacteria elicit PMN-endothelial cell interactions distinct from those seen when purified bacterial products are used as agonists.
authors.affiliation: Division of Pediatric Critical Care, Department of Pediatrics, University of Iowa, and Veterans Affairs Medical Center, Iowa City, IA 52242, USA. jessica-moreland@uiowa.edu
authors.forename: Jessica G
authors.initials: JG
authors.lastname: Moreland
authors.forename: Gail
authors.initials: G
authors.lastname: Bailey
authors.forename: William M
authors.initials: WM
authors.lastname: Nauseef
authors.forename: Jerrold P
authors.initials: JP
authors.lastname: Weiss
mesh_terms: D000328:Adult; D019138:Antibodies, Blocking / Q000494:pharmacology; D018821:CD18 Antigens / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002450:Cell Communication / Q000276:immunology*; D002460:Cell Line; D018925:Chemokines / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000166:cytology* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D004926:Escherichia coli / Q000502:physiology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D020556:Neutrophil Infiltration / Q000276:immunology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D013045:Species Specificity; D013211:Staphylococcus aureus / Q000502:physiology*; D013296:Streptococcus pneumoniae / Q000502:physiology*; D015854:Up-Regulation / Q000502:physiology
chemical_list: D019138:Antibodies, Blocking; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D018925:Chemokines; D008070:Lipopolysaccharides; D018799:Intercellular Adhesion Molecule-1