FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia
- Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD 21205 (United States)
- Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205 (United States)
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-{alpha}. Mitogen-activated protein kinases, ERK and p-38, and nuclear factor-{kappa}B 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.
- OSTI ID:
- 20710947
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 334, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2005.06.180; PII: S0006-291X(05)01426-9; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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