FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia

Jongseok Lee, Sooan Shin, Ching-Hao Teng, Jin Hong Suk, Sik Kim Kwang

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The generation of intense inflammation in the subarachnoid space in response to meningitis-causing bacteria contributes to brain dysfunction and neuronal injury in bacterial meningitis. Microglia, the major immune effector cells in the central nervous system (CNS), become activated by bacterial components to produce proinflammatory immune mediators. In this study, we showed that FimH adhesin, a tip component of type 1 fimbriae of meningitis-causing Escherichia coli K1, activated the murine microglial cell line, BV-2, which resulted in the production of nitric oxide and the release of tumor necrosis factor-α. Mitogen-activated protein kinases, ERK and p-38, and nuclear factor-κB were involved in FimH adhesin-mediated microglial activation. These findings suggest that FimH adhesin contributes to the CNS inflammatory response by virtue of activating microglia in E. coli meningitis.

Original languageEnglish
Pages (from-to)917-923
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume334
Issue number3
DOIs
Publication statusPublished - 2005 Sep 2

Fingerprint

Escherichia coli Adhesins
Escherichia coli Meningitis
Microglia
Neurology
Escherichia coli
Central Nervous System
Subarachnoid Space
Bacterial Meningitides
Mitogen-Activated Protein Kinases
Meningitis
Brain
Bacteria
Nitric Oxide
Tumor Necrosis Factor-alpha
Chemical activation
Cells
Inflammation
Cell Line
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Lee, Jongseok ; Shin, Sooan ; Teng, Ching-Hao ; Suk, Jin Hong ; Kwang, Sik Kim. / FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia. In: Biochemical and Biophysical Research Communications. 2005 ; Vol. 334, No. 3. pp. 917-923.
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FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia. / Lee, Jongseok; Shin, Sooan; Teng, Ching-Hao; Suk, Jin Hong; Kwang, Sik Kim.

In: Biochemical and Biophysical Research Communications, Vol. 334, No. 3, 02.09.2005, p. 917-923.

Research output: Contribution to journalArticle

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AB - The generation of intense inflammation in the subarachnoid space in response to meningitis-causing bacteria contributes to brain dysfunction and neuronal injury in bacterial meningitis. Microglia, the major immune effector cells in the central nervous system (CNS), become activated by bacterial components to produce proinflammatory immune mediators. In this study, we showed that FimH adhesin, a tip component of type 1 fimbriae of meningitis-causing Escherichia coli K1, activated the murine microglial cell line, BV-2, which resulted in the production of nitric oxide and the release of tumor necrosis factor-α. Mitogen-activated protein kinases, ERK and p-38, and nuclear factor-κB were involved in FimH adhesin-mediated microglial activation. These findings suggest that FimH adhesin contributes to the CNS inflammatory response by virtue of activating microglia in E. coli meningitis.

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