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Cited by 301

The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.

Iron acquisition and virulence in Helicobacter pylori: a major role for FeoB, a high‐affinity ferrous iron transporter

Open access
Velayudhan, Jyoti, Hughes, Nicky J., McColm, Andrew A., Bagshaw, Julie, Clayton, Chris L., Andrews, Simon C., Kelly, David J.·2000·Molecular Microbiology
DOI 10.1046/j.1365-2958.2000.01987.x
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Abstract

The genome sequence of Helicobacter pylori suggests that this bacterium possesses several Fe acquisition systems, including both Fe 2+‐ and Fe 3+‐citrate transporters. The role of these transporters was investigated by generating insertion mutants in feoB, tonB, fecA1 and fecDE. Fe transport in the feoB mutant was ≈ 10‐fold lower than in the wild type (with 0.5 μM Fe), irrespective of whether Fe was supplied in the Fe 2+ or Fe 3+ form. In contrast, transport rates were unaffected by the other mutations. Complementation of the feoB mutation fully restored both Fe 2+ and Fe 3+ transport. The growth inhibition exhibited by the feoB mutant in Fe‐deficient media was relieved by human holo‐transferrin, holo‐lactoferrin and Fe 3+‐dicitrate, but not by FeSO 4. The feoB mutant had less cellular Fe and was more sensitive to growth inhibition by transition metals in comparison with the wild type. Biphasic kinetics of Fe 2+ transport in the wild type suggested the presence of high‐ and low‐affinity uptake systems. The high‐affinity system (apparent Ks = 0.54 μM) is absent in the feoB mutant. Transport via FeoB is highly specific for Fe 2+ and was inhibited by FCCP, DCCD and vanadate, indicating an active process energized by ATP. Ferrozine inhibition of Fe 2+ and Fe 3+ uptake implied the concerted involvement of both an Fe 3+ reductase and FeoB in the uptake of Fe supplied as Fe 3+. Taken together, the results are consistent with FeoB‐mediated Fe 2+ uptake being a major pathway for H. pylori Fe acquisition. feoB mutants were unable to colonize the gastric mucosa of mice, indicating that FeoB makes an important contribution to Fe acquisition by H. pylori in the low‐pH, low‐O 2 environment of the stomach.

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Metadata

Authors
Velayudhan, J., Hughes, N. J., McColm, A. A., Bagshaw, J., Clayton, C. L., Andrews, S. C., & Kelly, D. J.
Venue
Molecular Microbiology
Publisher
Wiley
Published
2000-07
Volume
37
Issue
2
Pages
274-286
ISSN
  • 0950-382X (ISSN-L)
  • 1365-2958
DOI
10.1046/j.1365-2958.2000.01987.x
OpenAlex
W2042389184
Cited by
301
References
39
FWCI
14.68
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Iron acquisition and virulence in Helicobacter pylori: a major role for FeoB, a high‐affinity ferrous iron transporter. https://app.cochat.ai/papers/10.1046/j.1365-2958.2000.01987.x
The paper
Velayudhan, J., Hughes, N. J., McColm, A. A., Bagshaw, J., Clayton, C. L., Andrews, S. C., & Kelly, D. J. (2000). Iron acquisition and virulence in Helicobacter pylori: a major role for FeoB, a high‐affinity ferrous iron transporter. Molecular Microbiology. https://doi.org/10.1046/j.1365-2958.2000.01987.x

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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