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 journalArticlepeer-review

9 Scopus citations


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 (US)
Pages (from-to)917-923
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Sep 2 2005


  • Bacterial
  • E. Coli
  • Inflammation
  • Mitogen-activated protein kinases
  • Monocytes/macrophages
  • Nitric oxide
  • Nuclear factor-κB
  • Signal transduction
  • TNF-α

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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