Tumour necrosis factor-alpha causes an increase in blood-brain barrier permeability during sepsis

J Med Microbiol. 2001 Sep;50(9):812-821. doi: 10.1099/0022-1317-50-9-812.

Abstract

Blood-brain barrier (BBB) permeability during sepsis with Escherichia coli or Streptococcus pneumoniae was examined in a mouse model and measured by a circulating beta-galactosidase tracer. The leakage of brain microvascular vessels during sepsis was confirmed by transmission electron microscopic examination of brain tissues stained with horseradish peroxidase. The increase of BBB permeability induced by E. coli and S. pneumoniae, which was maximal at 3 h and 12 h after injection, respectively, was transient because of rapid clearance of the bacteria from the blood. Tumour necrosis factor-alpha (TNF-alpha) was stained on microvascular vessels of the brain during sepsis and intravenous injection of recombinant TNF-alpha also increased the BBB permeability. The increase in BBB permeability induced by either E. coli or S. pneumoniae could be inhibited by anti-TNF-alpha antibody. It was concluded that circulating TNF-alpha generated during sepsis induced the increase in BBB permeability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood-Brain Barrier / physiology*
  • Brain / immunology
  • Brain / ultrastructure
  • Disease Models, Animal
  • Escherichia coli / physiology
  • Escherichia coli Infections / immunology
  • Escherichia coli Infections / metabolism*
  • Female
  • Humans
  • Immunohistochemistry
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Electron
  • Pneumococcal Infections / immunology
  • Pneumococcal Infections / metabolism*
  • Sepsis / immunology
  • Sepsis / metabolism*
  • Streptococcus pneumoniae / physiology
  • Tumor Necrosis Factor-alpha / analysis
  • Tumor Necrosis Factor-alpha / physiology*
  • beta-Galactosidase / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • beta-Galactosidase