FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia.
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-kappaB 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.
Lee
Jongseok
J
Division of Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Shin
Sooan
S
Teng
Ching-Hao
CH
Hong
Suk Jin
SJ
Kim
Kwang Sik
KS
D018830:Adhesins, Escherichia coli / Q000502:physiology*; D000818:Animals; D002460:Cell Line; D004926:Escherichia coli / Q000502:physiology*; D036781:Fimbriae Proteins / Q000502:physiology*; D051379:Mice; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D018830:Adhesins, Escherichia coli; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C058769:fimH protein, E coli; D036781:Fimbriae Proteins; D009569:Nitric Oxide; D020928:Mitogen-Activated Protein Kinases