TNFα-induced cyclooxygenase 2 not only increases the vasopermeability of blood-brain barrier but also enhances the neutrophil survival in Escherichia coli-induced brain inflammation

Nina Tsao, Hui-Ping Hsu, Huan Yao Lei

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

In Escherichia coli-induced brain inflammation, cyclooxygenase-2 was induced not only on brain arterioles at 3 h, but also on infiltrating neutrophils at 9 h post-intracerebral injection. Intravenous injection of E. coli or recombinant TNFα also induced cyclooxygenase-2 expression on arterioles. Cyclooxygenase-2 and TNFα were co-localized on the arterioles as well as the infiltrating neutrophils by serial-section staining, indicating that cyclooxygenase-2 was induced by TNFα. NS398 (a cyclooxygenase-2 selective inhibitor) not only inhibited the increase of blood-brain barrier permeability, but also enhanced the apoptosis of the infiltrating neutrophils after E. coli stimulation. This suggests that TNFα-stimulated cyclooxygenase-2 induction play an important role on E. coli-induced brain inflammation. Its inhibition would help the resolution of neutrophil-mediated brain inflammation. Copyright (C) 1999 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)371-382
Number of pages12
JournalProstaglandins and Other Lipid Mediators
Volume57
Issue number5-6
DOIs
Publication statusPublished - 1999 Jul 1

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Encephalitis
Cyclooxygenase 2
Blood-Brain Barrier
Escherichia coli
Brain
Neutrophils
Arterioles
Cyclooxygenase 2 Inhibitors
Intravenous Injections
Permeability
Apoptosis
Staining and Labeling
Injections

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Cite this

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title = "TNFα-induced cyclooxygenase 2 not only increases the vasopermeability of blood-brain barrier but also enhances the neutrophil survival in Escherichia coli-induced brain inflammation",
abstract = "In Escherichia coli-induced brain inflammation, cyclooxygenase-2 was induced not only on brain arterioles at 3 h, but also on infiltrating neutrophils at 9 h post-intracerebral injection. Intravenous injection of E. coli or recombinant TNFα also induced cyclooxygenase-2 expression on arterioles. Cyclooxygenase-2 and TNFα were co-localized on the arterioles as well as the infiltrating neutrophils by serial-section staining, indicating that cyclooxygenase-2 was induced by TNFα. NS398 (a cyclooxygenase-2 selective inhibitor) not only inhibited the increase of blood-brain barrier permeability, but also enhanced the apoptosis of the infiltrating neutrophils after E. coli stimulation. This suggests that TNFα-stimulated cyclooxygenase-2 induction play an important role on E. coli-induced brain inflammation. Its inhibition would help the resolution of neutrophil-mediated brain inflammation. Copyright (C) 1999 Elsevier Science Inc.",
author = "Nina Tsao and Hui-Ping Hsu and Lei, {Huan Yao}",
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