ArticleMedical microbiology and immunology2008
Involvement of Escherichia coli K1 ibeT in bacterial adhesion that is associated with the entry into human brain microvascular endothelial cells.
Article in Medical microbiology and immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Vimentin-NF-κB signaling contributing to IbeA-mediated adhesion, invasion, and biofilm formation duringFrontiers in immunology · 2026Article
- Neonatal Meningitis-CausingInternational journal of molecular sciences · 2023Article
- Identification of novel genes involved in the biofilm formation process of Avian Pathogenic Escherichia coli (APEC).PloS one · 2022Article
- The role of major virulence factors and pathogenicity of adherent-invasivePrzeglad gastroenterologiczny · 2020Review
- The IbeA invasin of adherent-invasive Escherichia coli mediates interaction with intestinal epithelia and macrophages.Infection and immunity · 2015Article
- Article
- Some research advances of immune mechanism during infection in China.Science China. Life sciences · 2011Review
- Effects of ibeA deletion on virulence and biofilm formation of avian pathogenic Escherichia coli.Infection and immunity · 2011Article
- The GimA locus of extraintestinal pathogenic E. coli: does reductive evolution correlate with habitat and pathotype?PloS one · 2010Article
- Identification of protective and broadly conserved vaccine antigens from the genome of extraintestinal pathogenic Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Tentative identification of glycerol dehydrogenase as Escherichia coli K1 virulence factor cglD and its involvement in the pathogenesis of experimental neonatal meningitis.Medical microbiology and immunology · 2009Article
- Identification of IbeR as a stationary-phase regulator in meningitic Escherichia coli K1 that carries a loss-of-function mutation in rpoS.Journal of biomedicine & biotechnology · 2009Article
- Inactivation of ibeA and ibeT results in decreased expression of type 1 fimbriae in extraintestinal pathogenic Escherichia coli strain BEN2908.Infection and immunity · 2008Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
IbeT is a downstream gene of the invasion determinant ibeA in the chromosome of a clinical isolate of Escherichia coli K1 strain RS218 (serotype 018:K1:H7). Both ibeT and ibeA are in the same operon. Our previous mutagenesis and complementation studies suggested that ibeT may coordinately contribute to E. coli K1 invasion with ibeA. An isogenic in-frame deletion mutant of ibeT has been made by chromosomal gene replacement with a recombinant suicide vector carrying a fragment with an ibeT internal deletion. The characteristics of the mutant in meningitic E. coli infection were examined in vitro [cell culture of human brain microvascular endothelial cells (HBMEC)] and in vivo (infant rat model of E. coli meningitis) in comparison with the parent strain. The ibeT deletion mutant was significantly less adhesive and invasive than its parent strain E. coli E44 in vitro, and the adhesion- and invasion-deficient phenotypes of the mutant can be complemented by the ibeT gene. Recombinant IbeT protein is able to block E. coli E44 invasion of HBMEC. Furthermore, the ibeT deletion mutant is less capable of colonizing intestine and less virulent in bacterial translocation across the blood-brain barrier (BBB) than its parent E. coli E44 in vivo. These data suggest that ibeT-mediated E. coli K1 adhesion is associated with the bacterial invasion process.
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