Listeria monocytogenes infection and activation of human brain microvascular endothelial cells

J Infect Dis. 1998 Dec;178(6):1658-66. doi: 10.1086/314490.

Abstract

Listeria monocytogenes invasion of human brain microvascular endothelial cells (BMEC) and its role as a stimulus for endothelial cell activation were studied. Binding and invasion of intact BMEC monolayers were independent of the L. monocytogenes inlAB invasion locus. Cytochalasin D abrogated invasion of BMEC, whereas genistein effected only a 53% decrease in invasion, indicating a requirement for rearrangement of actin microfilaments but less dependence on tyrosine kinase activity. L. monocytogenes stimulated surface expression of E-selectin, ICAM-1, and to a lesser extent, VCAM-1, whereas L. monocytogenes prfA- and Deltahly mutants were severely compromised in this respect. Other experiments showed that BMEC infection stimulated monocyte and neutrophil adhesion and that CD18-mediated binding was the predominant mechanism for neutrophil adhesion to infected BMEC under static conditions. These data suggest that invasion of BMEC is a mechanism for triggering inflammation and leukocyte recruitment into the central nervous system during bacterial meningitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actin Cytoskeleton / physiology
  • Actin Cytoskeleton / ultrastructure
  • Actins / physiology
  • Actins / ultrastructure
  • Bacterial Adhesion / drug effects
  • Bacterial Adhesion / physiology*
  • Cells, Cultured
  • Cerebrovascular Circulation*
  • Cytochalasin D / pharmacology
  • E-Selectin / genetics
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / microbiology*
  • Endothelium, Vascular / physiology*
  • Gene Expression Regulation
  • Genistein / pharmacology
  • Humans
  • Intercellular Adhesion Molecule-1 / genetics
  • Listeria monocytogenes / genetics
  • Listeria monocytogenes / pathogenicity
  • Listeria monocytogenes / physiology*
  • Microcirculation
  • Protein-Tyrosine Kinases / metabolism
  • Vascular Cell Adhesion Molecule-1 / genetics

Substances

  • Actins
  • E-Selectin
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • Cytochalasin D
  • Genistein
  • Protein-Tyrosine Kinases