Arachidonic acid metabolism regulates Escherichia coli penetration of the blood-brain barrier

Infect Immun. 2010 Oct;78(10):4302-10. doi: 10.1128/IAI.00624-10. Epub 2010 Aug 9.

Abstract

Escherichia coli K1 meningitis occurs following penetration of the blood-brain barrier, but the underlying mechanisms involved in E. coli penetration of the blood-brain barrier remain incompletely understood. We have previously shown that host cytosolic phospholipase A(2)α (cPLA(2)α) contributes to E. coli invasion of human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier, but the underlying mechanisms remain unclear. cPLA(2)α selectively liberates arachidonic acid from membrane phospholipids. Here, we provide the first direct evidence that host 5-lipoxygenase and lipoxygenase products of arachidonic acid, cysteinyl leukotrienes (LTs), contribute to E. coli K1 invasion of HBMEC and penetration into the brain, and their contributions involve protein kinase C alpha (PKCα). These findings demonstrate that arachidonic acid metabolism regulates E. coli penetration of the blood-brain barrier, and studies are needed to further elucidate the mechanisms involved with metabolic products of arachidonic acid for their contribution to E. coli invasion of the blood-brain barrier.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Arachidonate 5-Lipoxygenase / metabolism
  • Arachidonic Acid / metabolism*
  • Blood-Brain Barrier / microbiology
  • Blood-Brain Barrier / physiology*
  • Brain / blood supply
  • Endothelial Cells / metabolism*
  • Escherichia coli / physiology*
  • Group IV Phospholipases A2 / metabolism
  • Humans
  • Leukotrienes / metabolism
  • Mice
  • Mice, Knockout
  • Protein Kinase C-alpha / metabolism

Substances

  • Leukotrienes
  • Arachidonic Acid
  • Arachidonate 5-Lipoxygenase
  • Protein Kinase C-alpha
  • Group IV Phospholipases A2