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• W2521799152 startingPage "e0162641" @default.
• W2521799152 abstract "Background NF-κB activation, pathogen invasion, polymorphonuclear leukocytes (PMN) transmigration (PMNT) across the blood-brain barrier (BBB) are the pathogenic triad hallmark features of bacterial meningitis, but the mechanisms underlying these events remain largely unknown. Vimentin, which is a novel NF-κB regulator, is the primary receptor for the major Escherichia coli K1 virulence factor IbeA that contributes to the pathogenesis of neonatal bacterial sepsis and meningitis (NSM). We have previously shown that IbeA-induced NF-κB signaling through its primary receptor vimentin as well as its co-receptor PTB-associated splicing factor (PSF) is required for pathogen penetration and leukocyte transmigration across the BBB. This is the first in vivo study to demonstrate how vimentin and related factors contributed to the pathogenic triad of bacterial meningitis. Methodology/Principal Findings The role of vimentin in IbeA+ E. coli K1-induced NF-κB activation, pathogen invasion, leukocyte transmigration across the BBB has now been demonstrated by using vimentin knockout (KO) mice. In the in vivo studies presented here, IbeA-induced NF-κB activation, E. coli K1 invasion and polymorphonuclear neutrophil (PMN) transmigration across the BBB were significantly reduced in Vim-/- mice. Decreased neuronal injury in the hippocampal dentate gyrus was observed in Vim-/- mice with meningitis. The major inflammatory regulator α7 nAChR and several signaling molecules contributing to NF-κB activation (p65 and p-CamKII) were significantly reduced in the brain tissues of the Vim-/- mice with E. coli meningitis. Furthermore, Vim KO resulted in significant reduction in neuronal injury and in α7 nAChR-mediated calcium signaling. Conclusion/Significance Vimentin, a novel NF-κB regulator, plays a detrimental role in the host defense against meningitic infection by modulating the NF-κB signaling pathway to increase pathogen invasion, PMN recruitment, BBB permeability and neuronal inflammation. Our findings provide the first evidence for Vim-dependent mechanisms underlying the pathogenic triad of bacterial meningitis." @default.
• W2521799152 created "2016-09-30" @default.
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• W2521799152 date "2016-09-22" @default.
• W2521799152 modified "2023-10-05" @default.
• W2521799152 title "Vimentin, a Novel NF-κB Regulator, Is Required for Meningitic Escherichia coli K1-Induced Pathogen Invasion and PMN Transmigration across the Blood-Brain Barrier" @default.
• W2521799152 cites W1521846222 @default.
• W2521799152 cites W1524284920 @default.
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• W2521799152 cites W1915617439 @default.
• W2521799152 cites W1968060691 @default.
• W2521799152 cites W1971810971 @default.
• W2521799152 cites W1981563557 @default.
• W2521799152 cites W1985130148 @default.
• W2521799152 cites W1986722064 @default.
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• W2521799152 cites W2003337475 @default.
• W2521799152 cites W2013617289 @default.
• W2521799152 cites W2014405748 @default.
• W2521799152 cites W2014846709 @default.
• W2521799152 cites W2022448990 @default.
• W2521799152 cites W2022770941 @default.
• W2521799152 cites W2024038175 @default.
• W2521799152 cites W2026244707 @default.
• W2521799152 cites W2028106813 @default.
• W2521799152 cites W2030784696 @default.
• W2521799152 cites W2033797312 @default.
• W2521799152 cites W2048047549 @default.
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• W2521799152 cites W2064979804 @default.
• W2521799152 cites W2067605157 @default.
• W2521799152 cites W2068971123 @default.
• W2521799152 cites W2069312908 @default.
• W2521799152 cites W2071577234 @default.
• W2521799152 cites W2073295417 @default.
• W2521799152 cites W2076247828 @default.
• W2521799152 cites W2077629366 @default.
• W2521799152 cites W2080476258 @default.
• W2521799152 cites W2092517967 @default.
• W2521799152 cites W2092530725 @default.
• W2521799152 cites W2093057561 @default.
• W2521799152 cites W2095531760 @default.
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• W2521799152 cites W2116984251 @default.
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• W2521799152 cites W2128380342 @default.
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• W2521799152 doi "https://doi.org/10.1371/journal.pone.0162641" @default.
• W2521799152 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5033352" @default.
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