Transcriptome of Escherichia coli K1 bound to human brain microvascular endothelial cells

Xie, Yi; Parthasarathy, Geetha; Cello, Francescopaolo Di; Teng, Ching Hao; Paul‐Satyaseela, Maneesh; Kim, Kwang Sik

doi:10.1016/j.bbrc.2007.10.174

Cited by 12 publications

(6 citation statements)

References 24 publications

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“…In contrast to IPECs, NMEC strains are associated with high mortality rates, are genetically closely related, express a number of well-characterized fitness factors and belong to only a few serotypes of which O18:K1:H7 is widely spread and the most studied serotype [ 71 ]. Transcriptome analysis has revealed that the expression level of the fliI gene is significantly increased in NMEC associated with HBMEC cells compared to NMEC not associated with cultured cells [ 72 ]. Further analysis indicated that the H7 flagellum of E. coli O18:K1:H7 may be involved in NMEC pathogenesis.…”

Section: Flagellum-mediated Adhesionmentioning

confidence: 99%

The Role of the Bacterial Flagellum in Adhesion and Virulence

Haiko

Westerlund-Wikström

2013

Biology

454

372

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The bacterial flagellum is a complex apparatus assembled of more than 20 different proteins. The flagellar basal body traverses the cell wall, whereas the curved hook connects the basal body to the whip-like flagellar filament that protrudes several µm from the bacterial cell. The flagellum has traditionally been regarded only as a motility organelle, but more recently it has become evident that flagella have a number of other biological functions. The major subunit, flagellin or FliC, of the flagellum plays a well-documented role in innate immunity and as a dominant antigen of the adaptive immune response. Importantly, flagella have also been reported to function as adhesins. Whole flagella have been indicated as significant in bacterial adhesion to and invasion into host cells. In various pathogens, e.g., Escherichia coli, Pseudomonas aeruginosa and Clostridium difficile, flagellin and/or the distally located flagellar cap protein have been reported to function as adhesins. Recently, FliC of Shiga-toxigenic E. coli was shown to be involved in cellular invasion via lipid rafts. Here, we examine the latest or most important findings regarding flagellar adhesive and invasive properties, especially focusing on the flagellum as a potential virulence factor.

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Section: Flagellum-mediated Adhesionmentioning

confidence: 99%

The Role of the Bacterial Flagellum in Adhesion and Virulence

Haiko

Westerlund-Wikström

2013

Biology

454

372

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“…A study comparing the gene expression patterns of HBMEC-associated versus non-associated E. coli with E. coli DNA microarray demonstrated that flagella play an important role in E. coli binding to HBMECs (66, 67). This concept is supported by the demonstration (a) that the mutant deleted of fliC was significantly defective in binding to and invasion of HBMECs, and this defect was restored by complementation with wild type fliC , (b) that recombinant flagellin (FliC) binds directly to the surface of HBMECs and (c) that exogenous recombinant flagellin inhibits E. coli binding to HBMECs (66).…”

Section: E Coli Penetration Of the Blood-brain Barriermentioning

confidence: 99%

“…The CGH was also utilized to examine the distribution of the eight RDIs that are relevant to the pathogenesis of E. coli meningitis among representative meningitis-causing E. coli isolates (67). RDI 16 harbors the K1 capsule biosynthesis gene cluster and, as expected, is present in all of the meningitis isolates.…”

Section: The Pathogenesis Of E Coli Meningitis: Functional Genomic Amentioning

confidence: 99%

Human Meningitis-Associated Escherichia coli

Kim

2016

EcoSal Plus

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E. coli is the most common Gram-negative bacillary organism causing meningitis and E. coli meningitis continues to be an important cause of mortality and morbidity throughout the world. Our incomplete knowledge of its pathogenesis contributes to such mortality and morbidity. Recent reports of E. coli strains producing CTX-M-type or TEM-type extended-spectrum β-lactamases create a challenge. Studies using in vitro and in vivo models of the blood-brain barrier have shown that E. coli meningitis follows a high-degree of bacteremia and invasion of the blood-brain barrier. E. coli invasion of the blood-brain barrier, the essentials step in the development of E. coli meningitis, requires specific microbial and host factors as well as microbe- and host-specific signaling molecules. Blockade of such microbial and host factors contributing to E. coli invasion of the blood-brain barrier is shown to be efficient in preventing E. coli penetration into the brain. The basis for requiring a high-degree of bacteremia for E. coli penetration of the blood-brain barrier, however, remains unclear. Continued investigation on the microbial and host factors contributing to a high-degree of bacteremia and E. coli invasion of the blood-brain barrier is likely to identify new targets for prevention and therapy of E. coli meningitis.

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“…Thus, ability to resist serum is likely an important virulence trait for both NMEC and APEC [9]. Although transcriptome and proteome approaches have been used to explore ExPEC pathogenesis [10][11][12][13][14][15], such approaches have rarely been used to probe ExPEC host specificity [16].…”

Section: Introductionmentioning

confidence: 99%