ArticleThe Journal of biological chemistry2022
In vivo growth of Staphylococcus lugdunensis is facilitated by the concerted function of heme and non-heme iron acquisition mechanisms.
Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Regulation of iron ion homeostasis inmBio · 2026Review
- A landscape of metallophore synthesis and uptake potential of the genusNAR genomics and bioinformatics · 2025Article
- Pheno- and genotypic iron acquisition of non-aureus staphylococci: a scoping review of literature with a focus on bovine mastitis.Veterinary research · 2025Article
- Indolenine-substituted pyrazole derivative 4e inhibits planktonicAntimicrobial agents and chemotherapy · 2025Article
- Drug Susceptibility, Siderophore Production, and Genome Analysis ofAntibiotics (Basel, Switzerland) · 2025Article
- Article
- The Staphylococcus aureus-antagonizing human nasal commensal Staphylococcus lugdunensis depends on siderophore piracy.Microbiome · 2024Article
- Genomic exploration of the fermented meat isolate Staphylococcus shinii IMDO-S216 with a focus on competitiveness-enhancing secondary metabolites.BMC genomics · 2024Article
- Phenotypic and genotypic assessment of iron acquisition in diverse bovine-associated non-aureus staphylococcal strains.Veterinary research · 2024Article
- Heme utilization by the enterococci.FEMS microbes · 2024Review
- Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.Infection and immunity · 2023Article
- Article
- Staphylococcus lugdunensis Uses the Agr Regulatory System to Resist Killing by Host Innate Immune Effectors.Infection and immunity · 2022Article
- The response of cecal microbiota to inflammatory state induced byFrontiers in microbiology · 2022Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus lugdunensis has increasingly been recognized as a pathogen that can cause serious infection indicating this bacterium overcomes host nutritional immunity. Despite this, there exists a significant knowledge gap regarding the iron acquisition mechanisms employed by S. lugdunensis, especially during infection of the mammalian host. Here we show that S. lugdunensis can usurp hydroxamate siderophores and staphyloferrin A and B from Staphylococcus aureus. These transport activities all required a functional FhuC ATPase. Moreover, we show that the acquisition of catechol siderophores and catecholamine stress hormones by S. lugdunensis required the presence of the sst-1 transporter-encoding locus, but not the sst-2 locus. Iron-dependent growth in acidic culture conditions necessitated the ferrous iron transport system encoded by feoAB. Heme iron was acquired via expression of the iron-regulated surface determinant (isd) locus. During systemic infection of mice, we demonstrated that while S. lugdunensis does not cause overt illness, it does colonize and proliferate to high numbers in the kidneys. By combining mutations in the various iron acquisition loci (isd, fhuC, sst-1, and feo), we demonstrate that only a strain deficient for all of these systems was attenuated in its ability to proliferate to high numbers in the murine kidney. We propose the concerted action of heme and non-heme iron acquisition systems also enable S. lugdunensis to cause human infection.
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