What question did this study set out to answer?

To review the mechanisms by which pathogenic bacteria capture iron from host carriers and regulate gene expression to withstand host nutritional immunity.

October 1, 2000Annual Review of Microbiology

Iron Metabolism in Pathogenic Bacteria

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Authors

CRColin RatledgeUniversity of Hull LDLynn G. DoverNorthumbria University

Discussion

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Implication

Review demonstrates diverse iron acquisition mechanisms and Fur-mediated gene regulation in pathogenic bacteria, suggesting novel targets for antimicrobial therapeutics.

Key Points

To review the mechanisms by which pathogenic bacteria capture iron from host carriers and regulate gene expression to withstand host nutritional immunity.
Evaluated host iron-withholding defense mechanisms, including sequestration by host proteins and Nramp1-mediated reactive oxygen species production.
Analyzed bacterial iron-scavenging pathways, including siderophore secretion, surface extraction, and heme internalization.
Examined Fe(II)-dependent transcriptional regulation mediated by the ferric uptake regulator (Fur) protein.
Pathogenic bacteria bypass host iron restriction by secreting high-affinity iron chelators (siderophores) or binding directly to host transferrin, ferritin, and hemoglobin.
Fluctuations in intracellular Fe(II) concentration govern the transcriptional control of more than 40 genes via the Fur repressor protein or its functional equivalents.
Targeting bacterial iron uptake and regulatory machinery represents a viable chemotherapeutic strategy against bacterial infections.

Cite This Study

Ratledge et al. (2000) studied this question.

synapsesocial.com/papers/69dbd8f33d9adb00e7685461 https://doi.org/10.1146/annurev.micro.54.1.881

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October 1, 2000Annual Review of Microbiology

Iron Metabolism in Pathogenic Bacteria

View Full Paper

Ask AI

Bookmark

Authors

CRColin RatledgeUniversity of Hull LDLynn G. DoverNorthumbria University

Discussion

Member takes

Implication

Review demonstrates diverse iron acquisition mechanisms and Fur-mediated gene regulation in pathogenic bacteria, suggesting novel targets for antimicrobial therapeutics.

Key Points

To review the mechanisms by which pathogenic bacteria capture iron from host carriers and regulate gene expression to withstand host nutritional immunity.
Evaluated host iron-withholding defense mechanisms, including sequestration by host proteins and Nramp1-mediated reactive oxygen species production.
Analyzed bacterial iron-scavenging pathways, including siderophore secretion, surface extraction, and heme internalization.
Examined Fe(II)-dependent transcriptional regulation mediated by the ferric uptake regulator (Fur) protein.
Pathogenic bacteria bypass host iron restriction by secreting high-affinity iron chelators (siderophores) or binding directly to host transferrin, ferritin, and hemoglobin.
Fluctuations in intracellular Fe(II) concentration govern the transcriptional control of more than 40 genes via the Fur repressor protein or its functional equivalents.
Targeting bacterial iron uptake and regulatory machinery represents a viable chemotherapeutic strategy against bacterial infections.

Cite This Study

Ratledge et al. (2000) studied this question.

synapsesocial.com/papers/69dbd8f33d9adb00e7685461 https://doi.org/10.1146/annurev.micro.54.1.881

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