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

doi:10.1016/j.bbrc.2005.06.180

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

School of Medicine

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

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 language	English (US)
Pages (from-to)	917-923
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	334
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2005.06.180
State	Published - Sep 2 2005

Keywords

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

Access to Document

10.1016/j.bbrc.2005.06.180

Cite this

@article{8c9bd50b1b754eb88139b85e7743a0ef,

title = "FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia",

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.",

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

author = "Jongseok Lee and Sooan Shin and Teng, {Ching Hao} and Suk, {Jin Hong} and Kwang, {Sik Kim}",

note = "Funding Information: This work was supported by National Institutes of Health Grants NS-26310 and AI47225, and in part by the Post-doctoral Fellowship Program of Korea Science and Engineering Foundation (KOSEF) for J.L. and we thank Dr. Michael McKinney (Mayo Clinic, Jacksonville, FL) for providing the BV-2 cell line and Dr. David Gally (University of Edinbugh, UK) for providing NEC026 strain. ",

year = "2005",

month = sep,

day = "2",

doi = "10.1016/j.bbrc.2005.06.180",

language = "English (US)",

volume = "334",

pages = "917--923",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "3",

}

TY - JOUR

T1 - FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia

AU - Lee, Jongseok

AU - Shin, Sooan

AU - Teng, Ching Hao

AU - Suk, Jin Hong

AU - Kwang, Sik Kim

N1 - Funding Information: This work was supported by National Institutes of Health Grants NS-26310 and AI47225, and in part by the Post-doctoral Fellowship Program of Korea Science and Engineering Foundation (KOSEF) for J.L. and we thank Dr. Michael McKinney (Mayo Clinic, Jacksonville, FL) for providing the BV-2 cell line and Dr. David Gally (University of Edinbugh, UK) for providing NEC026 strain.

PY - 2005/9/2

Y1 - 2005/9/2

N2 - 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.

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.

KW - Bacterial

KW - E. Coli

KW - Inflammation

KW - Mitogen-activated protein kinases

KW - Monocytes/macrophages

KW - Nitric oxide

KW - Nuclear factor-κB

KW - Signal transduction

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=22744444322&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=22744444322&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2005.06.180

DO - 10.1016/j.bbrc.2005.06.180

M3 - Article

C2 - 16036224

AN - SCOPUS:22744444322

SN - 0006-291X

VL - 334

SP - 917

EP - 923

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

IS - 3

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this