期刊
INFECTION AND IMMUNITY
卷 70, 期 7, 页码 3419-3426出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.70.7.3419-3426.2002
关键词
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资金
- NIAID NIH HHS [R01 AI050669, AI 50669, AI25096, R01 AI025096, R56 AI050669, R37 AI025096] Funding Source: Medline
The gram-negative enteric pathogen Vibrio cholerae requires iron for growth. V. cholerae has multiple iron acquisition systems, including utilization of heme and hemoglobin, synthesis and transport of the catechol siderophore vibriobactin, and transport of several siderophores that it does not itself make. One siderophore that V cholerae transports, but does not make, is enterobactin. Enterobactin transport requires TonB and is independent of the vibriobactin receptor ViuA. In this study, two candidate enterobactin receptor genes, irgA (VC0475) and vctA (VCA0232), were identified by analysis of the V. cholerae genomic sequence. A single mutation in either of these genes did not significantly impair enterobactin utilization, but a strain defective in both genes did not use enterobactin. When either irgA or vctA was supplied on a plasmid, the ability of the irgA vctA double mutant to use enterobactin was restored. This indicates that both VctA and IrgA transport enterobactin. We also identify the genes vctPDGC, which are linked to vctA and encode a periplasmic binding protein-dependent ABC transport system that functions in the utilization of both enterobactin and vibriobactin (VCA0227-0230). An irgA::TnphoA mutant strain, MBG40, was shown, in a previous study to be highly attenuated and to have a strong colonization defect in an infant mouse model of K. cholerae infection (M. B. Goldberg, V.J. DiRita, and S. B. Calderwood, Infect. Immun. 58:55-60, 1990). In this work, a new irg,4 mutation was constructed, and this mutant strain was not significantly impaired in its ability to compete with the parental strain in infant mice and was not attenuated for virulence in an assay of 50% lethal dose. These data indicate that the virulence defect in MBG40 is not due to the loss of irgA function and that irgA is unlikely to be an important virulence factor.
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