Disease relevance of Vibrio

• Genes in Escherichia coli and Vibrio parahaemolyticus were mutagenized, and mutants containing transposon-generated lux gene fusions produced light as a function of target gene transcription [1].
• This review uses the framework of the polar flagellar system of Vibrio parahaemolyticus to provide a synthesis of what is known about polar motility systems of the Vibrionaceae [2].
• Fourteen sporadic cases of non-O group 1 Vibrio cholerae gastroenteritis were identified through isolates submitted to the Centers for Disease Control in 1979 [3].
• This stimulation has been demonstrated in aldehyde mutants of two species of luminous bacteria, Beneckea harveyi and Photobacterium fischeri [4].
• In toxigenic isolates of Vibrio cholerae, tandem arrays of prophage DNA, usually interspersed with the related genetic element RS1, are integrated site-specifically within the chromosome [5].

High impact information on Vibrio

• We studied the clinical characteristics and epidemiology of disease associated with a rare, unnamed halophilic lactose-fermenting Vibrio species in 39 persons from whom the organism had been isolated [6].
• Here we investigate the role of Hsp104 in vivo using a temperature-sensitive Vibrio harveyi luciferase-fusion protein as a test substrate [7].
• Polar and lateral flagellar motors of marine Vibrio are driven by different ion-motive forces [8].
• Vibrio cholerae, the agent of epidemic and endemic cholera, colonizes the small bowel and secretes a potent enterotoxin that consists of a single A subunit, which stimulates adenylate cyclase activity, and five identical B subunits which bind to the ganglioside GM1 receptor of intestinal mucosal cells [9].
• Vibrio cholerae bacteria of the serological variety O1 were consistently isolated from water samples by passing the water with added Tween 20 through columns packed with polystyrene beads coated with antibodies against the O1 antigenic determinants [10].

Chemical compound and disease context of Vibrio

• In contrast, platelets that had been treated with Vibrio cholerae neuraminidase and from which 55% of total sialic acid had been removed were not lyzed in autologous serum and did not bind C3 as shown in binding assays using radiolabeled monoclonal anti-C3 antibody [11].
• Neuraminidase (Vibrio cholerae) treatment of human metastatic mammary carcinoma MDA-MB-231 cells grown in culture released 0.60-0.63 mg of N-acetylneuraminic acid from 10(9) cells [12].
• Human Factor VIII desialylated by treatment with Vibrio cholerae neuraminidase (ASVIII) aggregated human platelets in the absence of ristocetin in platelet-rich plasma and, to a lesser extent, in washed platelet suspensions [13].
• 110 El Tor Vibrio cholerae isolates from 102 patients with cholera between November, 1977, and March, 1978, during the early stages of the fourth epidemic of cholera in Tanzania had minimum inhibitory concentrations to tetracycline, chloramphenicol, nitrofurantoin, neomycin, ampicillin, and sulphadimidine determined [14].
• Polymyxin B sensitive strains of Vibrio cholerae non-O1 from recent epidemic in India [15].

Biological context of Vibrio

• The Vibrio cholerae O139 serogroup antigen includes an O-antigen capsule and lipopolysaccharide virulence determinants [16].
• The chromosomal replication origin (oriC) of Vibrio harveyi has been isolated on a plasmid and shown to function as an origin in Escherichia coli [17].
• Mechanisms for negative regulation by iron of the fatA outer membrane protein gene expression in Vibrio anguillarum 775 [18].
• The generation of CCCP-resistant membrane potential was inhibited by 2-heptyl-4-hydroxyquinoline-N-oxide that is known to inhibit the Na+-motive NADH oxidase of Vibrio alginolyticus [19].
• Despite this sequence variation, substrate specificity was broadly conserved, and L/F-transferase homologs from Providencia stuartii, Vibrio cholerae, Neisseria gonorrhoeae, and the cyanobacterium Synechocystis sp. all complemented an E. coli aat mutant (lacking L/F-transferase activity) for the degradation of N-end rule substrates [20].

Anatomical context of Vibrio

• The spleen, liver, or erythrocytes from adult A/J mice did not possess the antigen, but incubation of adult spleen or liver with neuraminidase (Vibrio cholerae) exposed the epitope [21].
• Intracutaneous injection of cholera toxin, exotoxin of Vibrio cholerae, into the dorsal skin of mice, rats, and hamsters at doses of greater than 0.1 ng evoked an acute reaction at the site of injection, which was characterized histologically by an edematous reaction in the dermis and mitotic stimulation in the epidermis [22].
• Conditions were developed for treating the isolated plasma membranes with Vibrio cholerae neuraminidase (VCN) so that 88% of the N-acetylneuraminic acid was removed without changing membrane proteins or other membrane carbohydrate constituents [23].
• Therefore, membrane-bound sialic acid (released by Vibrio cholerae neuraminidase treatment), ectosialyltransferase activity, and total cellular glycosidase levels were measured in this cell line and compared with levels in its parent melanoma tumor cell line, B16-F10, which was selected for its enhanced ability to form tumor nodules [24].
• We have previously reported that the chitin catabolic cascade in Vibrio furnissii involves multiple signal transducing systems, and that mono- and disaccharide chemoreceptors/transporters are essential components of some of these systems [25].

Gene context of Vibrio

• Many strains of Vibrio cholerae produce a cytolysin (VCC) that forms oligomeric transmembrane pores in animal cells [26].
• The negative regulation of the expression of iron transport genes fatA and fatB in Vibrio anguillarum is mediated by a chromosome-encoded Fur protein and a plasmid pJM1-derived antisense RNA (RNAalpha), which is preferentially expressed under iron-rich conditions [27].
• We have recently reported the molecular cloning of a gene, gspK, in Vibrio cholerae that encodes a specific glucosamine kinase [28].
• Treatment of solubilized SRIF receptors with neuraminidase from Vibrio cholera abolished high affinity agonist binding to the receptors, whereas treatment of the receptor with neuraminidase from Newcastle disease virus did not affect [125I]MK 678 binding to the receptor [29].
• Vibrio vulnificus is killed by normal human blood but grows rapidly in blood from patients with hemochromatosis [30].

Analytical, diagnostic and therapeutic context of Vibrio

• Sequence analysis of the beta-N-acetylhexosaminidase gene of Vibrio vulnificus: evidence for a common evolutionary origin of hexosaminidases [31].
• Sugar transport by the marine chitinolytic bacterium Vibrio furnissii. Molecular cloning and analysis of the mannose/glucose permease [25].
• The Na(+)/galactose cotransporter (vSGLT) of Vibrio parahaemolyticus, tagged with C-terminal hexahistidine, has been purified to apparent homogeneity by Ni(2+) affinity chromatography and gel filtration [32].
• Using a highly sensitive high performance liquid chromatography sialic acid assay in conjunction with Vibrio cholerae sialidase, we find that none of these metastatic variants differ significantly in their overall levels of cell surface sialic acid [33].
• These techniques have been adapted by several laboratories to study the spatial and temporal patterns of virulence gene expression by organisms such as Salmonella typhimurium, Listeria monocytogenes, Yersinia entercolitica and Vibrio cholerae during infection of tissue culture or animal models of infection [34].

References